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Find video protocols related to scientific articles indexed in Pubmed.
Effect of frying oils on the postprandial endoplasmic reticulum stress in obese people.
Mol Nutr Food Res
PUBLISHED: 09-22-2014
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The addition of antioxidants to frying oil reduces postprandial oxidative stress and the inflammatory response. ER stress may trigger both inflammation and oxidative stress processes. We aimed to determine the biological effects of the intake of four models of frying oils on postprandial ER stress in peripheral blood mononuclear cells. Twenty obese people received four breakfasts following a randomized crossover design, consisting of muffins made with different oils (virgin olive oil (VOO), sunflower oil (SFO), and a mixture of seed oils (SFO/canola oil) with either dimethylpolysiloxane (SOD) or natural antioxidants from olives (SOP) added), which were previously subjected to 20 heating cycles. ER stress was assessed by measuring the mRNA levels of sXBP1, BiP, CRT, and CNX in peripheral blood mononuclear cells. Our study showed that the intake of the muffins made with SFO induced the postprandial increase of the mRNA levels of the ER stress-sensor sXBP1, and the ER stress related chaperones BiP and CRT (all p-values <0.05). The harmful effects associated with the use of SFO as frying oil, in terms of inflammatory response and postprandial oxidative stress, may be partially mediated by the induction of postprandial ER stress.
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MEDITERRANEAN DIET AND CARDIOVASCULAR RISK: BEYOND TRADITIONAL RISK FACTORS.
Crit Rev Food Sci Nutr
PUBLISHED: 08-13-2014
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SUMMARY A strict adherence to the Mediterranean Diet (MedDiet) has repeatedly been linked to a low risk of cardiovascular disease in several situations. Initially, the mechanisms considered as possible causes of this were based on the effects of this dietary pattern on the so-called traditional risk factors (especially lipids and blood pressure). However, the high relative reduction in the prevalence of cardiovascular morbidity and mortality were not proportional to the limited findings about regulation of those traditional risk factors. In addition to several studies confirming the above effects, current research on the MedDiet is being focused on defining its effects on non-traditional risk factors, such as endothelial function, inflammation, oxidative stress, or on controlling the conditions which predispose people to cardiovascular events, such as obesity, metabolic syndrome or type 2 diabetes mellitus. In the current article, after briefly reviewing the known effects of the MedDiet on the traditional risk factors, we will mainly focus on reviewing the current evidence about the effects that this dietary pattern exerts on alternative factors, including postprandial lipemia or coagulation, among others, as well as providing a short review on future directions.
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Elevated GH/IGF-I promotes mammary tumors in high-fat, but not low-fat, fed mice.
Carcinogenesis
PUBLISHED: 08-01-2014
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Growth hormone (GH) and/or insulin-like growth factor I (IGF-I) are thought to promote breast cancer based on reports showing circulating IGF-I levels correlate, in epidemiological studies, with breast cancer risk. Also, mouse models with developmental GH/IGF-I deficiency/resistance are less susceptible to genetic- or chemical-induced mammary tumorigenesis. However, given the metabolic properties of GH, medical strategies have been considered to raise GH to improve body composition and metabolic function in elderly and obese patients. Since hyperlipidemia, inflammation, insulin resistance and obesity increase breast cancer risk, elevating GH may serve to exacerbate cancer progression. To better understand the role GH/IGF-I plays in tumor formation, this study used unique mouse models to determine if reducing GH/IGF-I in adults protects against 7,12-dimethylbenz[?]anthracene (DMBA)-induced mammary tumor development, and if moderate elevations in endogenous GH/IGF-I alter DMBA-induced tumorigenesis in mice fed a standard-chow diet or in mice with altered metabolic function due to high-fat feeding. We observed that adult-onset isolated GH-deficient mice, which also have reduced IGF-I levels, were less susceptible to DMBA-treatment. Specifically, fewer adult-onset isolated GH-deficient mice developed mammary tumors compared with GH-replete controls. In contrast, chow-fed mice with elevated endogenous GH/IGF-I (HiGH mice) were not more susceptible to DMBA-treatment. However, high-fat-fed, HiGH mice showed reduced tumor latency and increased tumor incidence compared with diet-matched controls. These results further support a role of GH/IGF-I in regulating mammary tumorigenesis but suggest the ultimate consequences of GH/IGF-I on breast tumor development are dependent on the diet and/or metabolic status.
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Effects of the Mediterranean Diet Supplemented With Coenzyme Q10 on Metabolomic Profiles in Elderly Men and Women.
J. Gerontol. A Biol. Sci. Med. Sci.
PUBLISHED: 07-03-2014
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Characterization of the variations in the metabolomic profiles of elderly people is a necessary step to understand changes associated with aging. This study assessed whether diets with different fat quality and supplementation with coenzyme Q10 (CoQ) affect the metabolomic profile in urine analyzed by proton nuclear magnetic resonance spectroscopy from elderly people.
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Influence of endothelial dysfunction on telomere length in subjects with metabolic syndrome: LIPGENE study.
Age (Dordr)
PUBLISHED: 06-26-2014
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Previous evidences support that increased oxidative stress (OxS) may play an important role in metabolic syndrome (MetS) and both are closely linked to vascular dysfunction. This study determined whether there is a relationship between endothelial function and relative telomere length (RTL) in MetS subjects. In this cross-sectional study from the LIPGENE cohort, a total of 88 subjects (36 men and 52 women) were divided into four groups by quartiles of telomere length. We measured ischemic reactive hyperemia (IRH), total nitrite (NO) and protein carbonyl (PC) plasma levels, F2-isoprostanes urinary levels, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) plasma activities. IRH and NO plasma levels were higher in subjects with longer RTL (quartiles 3 and 4), while PC plasma levels, F2-isoprostanes urinary levels, and GPx and SOD plasma activities were lower in quartile 4 subjects (longest RTL). Additionally, MetS subjects with longer RTL had greater homeostatic model assessment-? level and lower triglycerides plasma levels. Our results suggest that endothelial dysfunction, associated with high levels of OxS, could be entailed in an increment of telomere attrition. Thus, further support of the molecular and cellular mechanisms involved in vascular dysfunction may contribute to the development of strategies to decelerate vascular aging or prevent cardiovascular disease.
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[Diagnosis and treatment of familial hypercholesterolemia in Spain: Consensus document.]
Semergen
PUBLISHED: 04-30-2014
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Familial hypercholesterolemia (FH) is a common genetic disorder, clinically manifested since birth, and associated with very high levels of plasma LDL-cholesterol (LDL-c), xanthomas, and premature coronary heart disease. Its early detection and treatment reduces coronary morbidity and mortality. Despite effective treatment being available, FH is under-diagnosed and under-treated. Identification of index cases and cascade screening using LDL-c levels and genetic testing are the most cost-effective strategies for detecting new cases and starting early treatment. Long-term treatment with statins has decreased the vascular risk to the levels of the general population. LDL-c targets are <130mg/dL for children and young adults, <100mg/dL for adults, and <70mg/dL for adults with known coronary heart disease or diabetes. Most patients do not to reach these goals, and combined treatments with ezetimibe or other drugs may be necessary. When the goals are not achieved with the maximum tolerated drug treatment, a reduction ?50% in LDL-c levels can be acceptable. Lipoprotein apheresis can be useful in homozygous, and in treatment-resistant severe heterozygous, cases. This Consensus Paper gives recommendations on the diagnosis, screening, and treatment of FH in children and adults, and specific advice to specialists and general practitioners with the objective of improving the clinical management of these patients, in order to reduce the high burden of coronary heart disease.
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[Diagnosis and treatment of familial hypercholesterolemia in Spain: Consensus document.]
Aten Primaria
PUBLISHED: 04-08-2014
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Familial hypercholesterolemia (FH) is a common genetic disorder, clinically manifested since birth, and associated with very high levels of plasma LDL-cholesterol (LDL-c), xanthomas, and premature coronary heart disease. Its early detection and treatment reduces coronary morbidity and mortality. Despite effective treatment being available, FH is under-diagnosed and under-treated. Identification of index cases and cascade screening using LDL-c levels and genetic testing are the most cost-effective strategies for detecting new cases and starting early treatment. Long-term treatment with statins has decreased the vascular risk to the levels of the general population. LDL-c targets are <130mg/dL for children and young adults, <100mg/dL for adults, and <70mg/dL for adults with known coronary heart disease or diabetes. Most patients do not to reach these goals, and combined treatments with ezetimibe or other drugs may be necessary. When the goals are not achieved with the maximum tolerated drug treatment, a reduction ?50% in LDL-c levels can be acceptable. Lipoprotein apheresis can be useful in homozygous, and in treatment-resistant severe heterozygous, cases. This Consensus Paper gives recommendations on the diagnosis, screening, and treatment of FH in children and adults, and specific advice to specialists and general practitioners with the objective of improving the clinical management of these patients, in order to reduce the high burden of coronary heart disease.
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Olive oil phenolic compounds decrease the postprandial inflammatory response by reducing postprandial plasma lipopolysaccharide levels.
Food Chem
PUBLISHED: 04-06-2014
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We investigated the molecular mechanisms by which phenolic compounds (phenols) in virgin olive oil reduce the postprandial inflammatory response with the aim of identifying the transcription factor involved and the downstream effects. Olive oil-based breakfasts prepared with virgin olive oil (VOO) with high (398 ppm), intermediate (149 ppm) and low (70 ppm) phenol content were administered to 49 metabolic syndrome patients following a randomized crossover design. The consumption of a high-phenol VOO-based breakfast limited the increase of lipopolysaccharide plasma levels, TLR4, and SOCS3 proteins (p<0.001, p=0.041 and p=0.008, respectively), the activation of NF-?B (p=0.016) and the IL6 (p=0.007 and p=0.048, low and intermediate oil, respectively), IL1B (p=0.002, intermediate oil), and CXCL1 (p=0.001) postprandial gene expression, in peripheral blood mononuclear cells, as compared with the consumption of a breakfast prepared with the same oil but with low or intermediate phenol content. Virgin olive oil phenolic compounds reduce the postprandial inflammatory response in association with postprandial plasma lipopolysaccharide levels.
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Peripheral blood mononuclear cells as in vivo model for dietary intervention induced systemic oxidative stress.
Food Chem. Toxicol.
PUBLISHED: 03-19-2014
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Our aim was to assess the use of peripheral blood mononuclear cells (PBMC) as an in vivo cellular model to evaluate diet-induced changes in the oxidative stress status by analyzing the gene expression pattern of NADPH-oxidase subunits and antioxidant genes. A randomized, controlled trial assigned metabolic syndrome patients to 4 diets for 12 weeks each: (i) high-saturated fatty acid (HSFA), (ii) high-monounsaturated fatty acid, and (iii), (iv) two low-fat, high-complex carbohydrate diets supplemented with n-3 polyunsaturated fatty acids or placebo. A fat challenge reflecting the fatty acid composition as the original diets was conducted post-intervention. The mRNA levels of gp91(phox) (P<0.001), p22(phox) (P=0.005), p47(phox) (P=0.001) and p40(phox) (P<0.001) increased at 2h after the intake of the HSFA meal. The expression of SOD1, SOD2, GSR, GPx1, GPX4, TXN, TXNRD1 and Nrf2 increased after the HSFA meal (p<0.05). In contrast, the expression of these genes remained unaltered in response to the other dietary interventions. Our results suggest that the increased expression of antioxidant genes in PBMC seems to be due to the response to the postprandial oxidative stress generated mainly in adipose tissue after the consumption of an HSFA diet.
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[Effect of two hypocaloric diets and their combination with physical exercise on basal metabolic rate and body composition].
Nutr Hosp
PUBLISHED: 02-25-2014
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Metabolic syndrome (MetS) is diagnosed by the detection of at least three criteria (hypertriglyceridemia, low HDL-C, hypertension, obesity and altered fasting glucose). Visceral fat excess would be the starting point for its development. Scientific evidence supports hypocaloric diets -mediterranean or low fat diet and rich in complex carbohydrates diet included- as the best treatment to reduce fat mass (FM), maximizing its impact by combining them with physical exercise (PE). However, the effects of these treatments on basal metabolic rate (BMR) of patients with MetS, are unknown.
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Polymorphism at the TNF-alpha gene interacts with Mediterranean diet to influence triglyceride metabolism and inflammation status in metabolic syndrome patients: From the CORDIOPREV clinical trial.
Mol Nutr Food Res
PUBLISHED: 02-20-2014
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To examine whether the consumption of a Mediterranean diet (MedDiet), compared with a low-fat diet, interacts with two single nucleotide polymorphisms at the tumor necrosis factor alpha gene (rs1800629, rs1799964) in order to improve triglycerides (TG), glycemic control, and inflammation markers.
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Dietary fat modifies lipid metabolism in the adipose tissue of metabolic syndrome patients.
Genes Nutr
PUBLISHED: 02-14-2014
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Adipose tissue (AT) is a key organ in the regulation of total body lipid homeostasis, which is responsible for the storage and release of fatty acids according to metabolic needs. We aimed to investigate the effect of the quantity and quality of dietary fat on the lipogenesis and lipolysis processes in the AT of metabolic syndrome (MetS) patients. A randomized, controlled trial conducted within the LIPGENE study assigned MetS patients to one of four diets: (a) high-saturated fatty acid (HSFA) (b) high-monounsaturated fatty acid, and (c, d) two low-fat, high-complex carbohydrate diets supplemented with long chain (LC) n-3 (LFHCC n-3) polyunsaturated fatty acids (PUFA) or placebo (LFHCC), for 12 weeks each. A fat challenge reflecting the same fatty acid composition as the original diets was conducted post-intervention. Long-term consumption of the LFHCC diet induced an increase in the fasting expression levels of the sterol regulatory element binding protein-1 and stearoyl-CoA desaturase D9-desaturase genes, whereas the supplementation of this diet with n-3 PUFA reversed this effect (p = 0.007). In contrast, long-term consumption of the HSFA diet increased the expression of the adipose triglyceride lipase (ATGL) gene, at both fasting and postprandial states (both, p < 0.001). Our results showed the anti-lipogenic effect exerted by LC n-3 PUFA when administered together with a LFHCC diet. Conversely, a diet high in saturated fat increased the expression of the lipolytic gene ATGL relative to the other diets.
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Metabolic phenotypes of obesity influence triglyceride and inflammation homoeostasis.
Eur. J. Clin. Invest.
PUBLISHED: 02-07-2014
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We examined the degree of postprandial triglyceride (TG) response over the day, representing a highly dynamic state, with continuous metabolic adaptations, among normal-weight, overweight and obese patients, according to their metabolically healthy or abnormal status.
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Dietary fat alters the expression of cortistatin and ghrelin systems in the PBMCs of elderly subjects: putative implications in the postprandial inflammatory response.
Mol Nutr Food Res
PUBLISHED: 01-28-2014
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Dietary fat influences systemic inflammatory status, which determines the progression of age-associated diseases. Since somatostatin (SST), cortistatin (CORT), and ghrelin systems modulate inflammatory response, we aim to comprehensively characterize the presence and regulation of the components of these systems in the peripheral blood mononuclear cells (PMBCs), a subset of white blood cells placed at the crossroad between diet and inflammation, in response to diets with different fat composition, and during the postprandial phase in elderly subjects.
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Beneficial effect of CLOCK gene polymorphism rs1801260 in combination with low-fat diet on insulin metabolism in the patients with metabolic syndrome.
Chronobiol. Int.
PUBLISHED: 12-11-2013
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Genetic variation at the Circadian Locomotor Output Cycles Kaput (CLOCK) locus has been associated with lifestyle-related conditions such as obesity, metabolic syndrome (MetS) and cardiovascular diseases. In fact, it has been suggested that the disruption of the circadian system may play a causal role in manifestations of MetS. The aim of this research was to find out whether habitual consumption of a low-fat diet, compared with a Mediterranean diet enriched with olive oil, modulates the associations between common CLOCK single nucleotide polymorphisms (SNPs) (rs1801260, rs3749474 and rs4580704) and lipid and glucose-related traits among MetS patients. Plasma lipid and insulin concentrations, indexes related with insulin resistance (homeostasis model assessment of insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI)) and CLOCK SNPs were determined in 475 MetS subjects participating in the CORDIOPREV clinical trial (NCT00924937). Gene-diet interactions were analyzed after a year of dietary intervention (Mediterranean diet (35% fat, 22% monounsaturated fatty acids (MUFA)) versus low-fat diet (28% fat, 12% MUFA)). We found significant gene-diet interactions between rs1801260 SNP and the dietary pattern for insulin concentrations (p?=?0.009), HOMA-IR (p?=?0.014) and QUICKI (p?=?0.028). Specifically, after 12 months of low-fat intervention, subjects who were homozygous for the major allele (TT) displayed lower plasma insulin concentrations (p?=?0.032), lower insulin resistance (HOMA-IR; p?=?0.027) and higher insulin sensitivity (QUICKI; p?=?0.024) compared with carriers of the minor allele C (TC?+?CC). In contrast, in the Mediterranean intervention group a different trend was observed although no significant differences were found between CLOCK genotypes after 12 months of treatment. Our data support the notion that a chronic consumption of a healthy diet may play a contributing role in triggering glucose metabolism by interacting with the rs1801260 SNP at CLOCK gene locus in MetS patients. Due to the complex nature of gene-environment interactions, dietary adjustment in subjects with the MetS may require a personalized approach.
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Nutrigenetics, Metabolic Syndrome Risk and Personalized Nutrition.
Curr Vasc Pharmacol
PUBLISHED: 10-31-2013
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The metabolic syndrome (MetS) is a constellation of metabolic risk factors reflecting overnutrition and sedentary lifestyle and its prevalence is increasing dramatically to epidemic proportions. The importance of MetS lies in its close association with the risk of cardiovascular disease and type 2 diabetes. In this scenario, the principal goals of pharmacological therapy for these patients are to achieve and maintain an optimal cardiometabolic control, including lipids, blood glucose and blood pressure; in order to prevent and treat potential complications. Moreover nutrition has commonly been accepted as a cornerstone of treatment for MetS, with the expectation that an appropriate intake of energy and nutrients will improve its control. However the question arises as to whether dietary therapy may require a more personalised approach. In this regard advances in high-throughput genetic analysis have improved our understanding of the contribution of genetics to this diet-related condition. In this review we will present the current state of the art illustrating the significance of gene-nutrient interactions in the context of MetS risk.
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Relevance of Postprandial Lipemia in Metabolic Syndrome.
Curr Vasc Pharmacol
PUBLISHED: 10-31-2013
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Metabolic Syndrome (MetS) is a complex disorder defined by the aggregation of interconnected cardiometabolic risk factors which increase the risk of diabetes mellitus type 2 and cardiovascular disease (CVD). MetS is currently a matter of concern and it will continue to be in the future, since there is likely to be a dramatic increase in its prevalence, and subjects with MetS will run an increased risk of mortality, mainly through CVD. Moreover, the implications on the global health burden and the worldwide epidemic of this complex disorder will impact greatly on socioeconomic cost. MetS is therefore a matter of serious concern and we need to understand its etiology in order to improve strategies of treatment and prevention. In this regard, postprandial lipemia has increased in importance over the last few years as it has been demonstrated to influence the development of atherosclerosis. In addition, in modern times, fasting is not the typical physiological state of humans; in fact, they spend most of the time in the postprandial state. However, although it is obvious that postprandial lipemia is present in conditions of obesity, little is known about the relevance of postprandial lipemia in MetS. In the current review, we will explore some aspects of postprandial lipemia which could be of interest for understanding the pathogenesis of this complex disorder and which may help us advance towards more personalized nutrition.
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Postprandial Activation of P53-Dependent DNA Repair Is Modified by Mediterranean Diet Supplemented With Coenzyme Q10 in Elderly Subjects.
J. Gerontol. A Biol. Sci. Med. Sci.
PUBLISHED: 10-24-2013
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Alterations in the expression levels of genes and proteins involved in oxidative stress and DNA damage response underlie the phenotypic changes associated with aging. We have investigated whether the quality of dietary fat alters postprandial gene expression and protein levels involved in p53-dependent DNA repair and whether the supplementation with Coenzyme Q10 improves this situation in an elderly population.
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An acute intake of a walnut-enriched meal improves postprandial adiponectin response in healthy young adults.
Nutr Res
PUBLISHED: 08-26-2013
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A deficit in adiponectin plays an important causal role in insulin resistance and metabolic syndrome. We hypothesized that as seen during the fasting state, the intake of a walnut-enriched meal increased postprandial adiponectin. Twenty-one healthy white men followed a 4-week baseline diet and then consumed 3 fat-loaded meals that included 1 g fat/kg body weight (65% fat) according to a randomized crossover design: olive oil-enriched meal (22% saturated fatty acids [SFA], 38% monounsaturated fatty acids [MUFA], 4% polyunsaturated fatty acids [PUFA]), butter-enriched meal (35% SFA, 22% MUFA, 4% PUFA), and walnut-enriched meal (20% SFA, 24% MUFA, 16% PUFA, and 4% ?-linolenic acid). Leptin, resistin, adiponectin, and free fatty acids were determined at 0, 3, 6, and 8.5 hours after the fat load. After the walnut-enriched meal, plasma adiponectin concentrations were higher at 3 and 6 hours (P = .011, P = .046, respectively) compared with the butter-enriched meal and higher at 6 hours compared with the olive oil-enriched meal (P = .036). Free fatty acid levels decreased from baseline at 3 hours after the walnut-enriched meal (P = .001). No differences were observed between the 3 meals for leptin and resistin responses. Our data confirmed a beneficial profile in the postprandial response to walnuts, source of omega-3 PUFA with an increased postprandial adiponectin and lower postprandial free fatty acid responses. These findings suggest that the postprandial state is important for understanding the possible cardioprotective effects associated with omega-3 PUFA dietary fat.
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Dietary fat differentially influences the lipids storage on the adipose tissue in metabolic syndrome patients.
Eur J Nutr
PUBLISHED: 07-26-2013
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Adipose tissue is now recognized as a highly active metabolic and endocrine organ. Our aim was to investigate the effect of the dietary fat on the two main adipose tissue functions, endocrine and lipid store, by analyzing the adipose tissue gene expression from metabolic syndrome patients.
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Oxidative stress is associated with the number of components of metabolic syndrome: LIPGENE study.
Exp. Mol. Med.
PUBLISHED: 06-22-2013
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Previous evidence supports the important role that oxidative stress (OxS) plays in metabolic syndrome (MetS)-related manifestations. We determined the relationship between the number of MetS components and the degree of OxS in MetS patients. In this comparative cross-sectional study from the LIPGENE cohort, a total of 91 MetS patients (43 men and 48 women; aged between 45 and 68 years) were divided into four groups based on the number of MetS components: subjects with 2, 3, 4 and 5 MetS components (n=20, 31, 28 and 12, respectively). We measured ischemic reactive hyperemia (IRH), plasma levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), total nitrite, lipid peroxidation products (LPO), hydrogen peroxide (H2O2), superoxide dismutase (SOD) and glutathione peroxidase (GPx) plasma activities. sVCAM-1, H2O2 and LPO levels were lower in subjects with 2 or 3 MetS components than subjects with 4 or 5 MetS components. IRH and total nitrite levels were higher in subjects with 2 or 3 MetS components than subjects with 4 or 5 MetS components. SOD and GPx activities were lower in subjects with 2 MetS components than subjects with 4 or 5 MetS components. Waist circumference, weight, age, homeostatic model assessment-?, triglycerides (TGs), high-density lipoprotein and sVCAM-1 levels were significantly correlated with SOD activity. MetS subjects with more MetS components may have a higher OxS level. Furthermore, association between SOD activity and MetS components may indicate that this variable could be the most relevant OxS biomarker in patients suffering from MetS and could be used as a predictive tool to determine the degree of the underlying OxS in MetS.
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Endothelial aging associated with oxidative stress can be modulated by a healthy mediterranean diet.
Int J Mol Sci
PUBLISHED: 03-05-2013
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Aging is a condition which favors the development of atherosclerosis, which has been associated with a breakdown in repair processes that occurs in response to cell damage. The dysregulation of the biological systems associated with aging are produced partly through damage which accumulates over time. One major source of this injury is oxidative stress, which can impair biological structures and the mechanisms by which they are repaired. These mechanisms are based on the pathogenesis of endothelial dysfunction, which in turn is associated with cardiovascular disease, carcinogenesis and aging. The dependent dysfunction of aging has been correlated with a reduction in the number and/or functional activity of endothelial progenitor cells, which could hinder the repair and regeneration of the endothelium. In addition, aging, inflammation and oxidative stress are endogenous factors that cause telomere shortening, which is dependent on oxidative cell damage. Moreover, telomere length correlates with lifestyle and the consumption of a healthy diet. Thus, diseases associated with aging and age may be caused by the long-term effects of oxidative damage, which are modified by genetic and environmental factors. Considering that diet is a very important source of antioxidants, in this review we will analyze the relationship between oxidative stress, aging, and the mechanisms which may be involved in a higher survival rate and a lower incidence of the diseases associated with aging in populations which follow a healthy diet.
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Antioxidant system response is modified by dietary fat in adipose tissue of metabolic syndrome patients.
J. Nutr. Biochem.
PUBLISHED: 02-12-2013
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Metabolic syndrome (MetS) is associated with high oxidative stress, which is caused by an increased expression of NADPH-oxidase and a decreased expression of antioxidant enzymes in the adipose tissue. Our aim was to evaluate whether the quality and quantity of dietary fat can modify that process. A randomized, controlled trial conducted within the LIPGENE study assigned MetS patients to one of four diets for 12 wk each: (i) high-saturated fatty acid (HSFA), (ii) high-monounsaturated fatty acid (HMUFA), (iii) and (iv) two low-fat, high-complex carbohydrate diet supplemented with n-3 polyunsaturated fatty acids (LFHCC n3), or placebo (LFHCC). A fat challenge reflecting the same fatty acid composition as the original diets was conducted post-intervention. The intake of an HSFA meal induced a higher postprandial increase in gp91phox and p67phox mRNA levels than after the intake of HMUFA, LFHCC and LFHCC n-3 meals (all p-values<0.05). The postprandial decrease in CAT, GPXs and TXNRD1 mRNA levels after the HSFA meal intake was higher than after the intake of HMUFA, LFHCC and LFHCC n-3 meals (all p-values<0.05). The intake of an HSFA meal induced a higher postprandial increase in KEAP1 mRNA levels than after the consumption of the HMUFA (P=.007) and LFHCC n-3 (P=.001) meals. Our study demonstrated that monounsaturated fat consumption reduces oxidative stress as compared to saturated fat by inducing higher postprandial antioxidant response in adipose tissue, and thus, replacing SFA for MUFA may be an effective dietary strategy to reduce the oxidative stress in MetS patients and its pathophysiological consequences.
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Postprandial oxidative stress is modulated by dietary fat in adipose tissue from elderly people.
Age (Dordr)
PUBLISHED: 01-23-2013
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We have investigated whether dietary fat modifies the postprandial oxidative stress in adipose tissue of elderly people. Twenty participants received three diets for 4 weeks each: SFA-rich diet, Mediterranean (Med) diet enriched in MUFA with virgin olive oil, and a low-fat, high-carbohydrate diet enriched in n-3 PUFA (?-linolenic acid from plant origin) (CHO-PUFA diet). After 12 h of fasting, volunteers received a breakfast reflecting the fatty acid composition of the diet ingested in the preceding dietary period. Med diet induced higher postprandial SOD2 and TrxR mRNA levels, and CHO-PUFA diet induced higher GPx1 and TrxR mRNA levels compared with SFA-rich diet. Med and CHO-PUFA breakfasts induced a postprandial increase in plasma reduced glutathione (GSH), and a greater postprandial GSH/oxidized glutathione ratio compared to the SFA-rich diet. Our study suggests that the consumption of Med and CHO-PUFA diets may reduce postprandial oxidative stress compared to an SFA-rich diet, which may be due to higher antioxidant enzymes gene expression in adipose tissue.
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Endoplasmic reticulum stress in adipose tissue determines postprandial lipoprotein metabolism in metabolic syndrome patients.
Mol Nutr Food Res
PUBLISHED: 01-15-2013
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Our aim was to ascertain whether the quality and quantity of fat in the diet may influence the ER stress at the postprandial state in adipose tissue by analyzing the gene expression of chaperones, folding enzymes, and activators of the UPR.
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Postprandial inflammatory response in adipose tissue of patients with metabolic syndrome after the intake of different dietary models.
Mol Nutr Food Res
PUBLISHED: 12-07-2011
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Dysfunctional adipose tissue may be an important trigger of molecular inflammatory pathways that cause cardiovascular diseases. Our aim was to determine whether the specific quality and quantity of dietary fat produce differential postprandial inflammatory responses in adipose tissue from metabolic syndrome (MetS) patients.
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Expression of proinflammatory, proatherogenic genes is reduced by the Mediterranean diet in elderly people.
Br. J. Nutr.
PUBLISHED: 11-15-2011
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Ageing is an important determinant of atherosclerosis development rate, mainly by the creation of a chronic low-grade inflammation. Diet, and particularly its fat content, modulates the inflammatory response in the fasting and postprandial states. Our aim was to study the effects of dietary fat on the expression of genes related to inflammation (NF-?B, monocyte chemoattractant protein 1 (MCP-1), TNF-? and IL-6) and plaque stability (matrix metalloproteinase 9, MMP-9) during the postprandial state of twenty healthy, elderly people who followed three diets for 3 weeks each: (1) Mediterranean diet (Med Diet) enriched in MUFA with virgin olive oil; (2) SFA-rich diet; and (3) low-fat, high-carbohydrate diet enriched in n-3 PUFA (CHO-PUFA diet) by a randomised crossover design. At the end of each period, after a 12-h fast, the subjects received a breakfast with a composition similar to the one when the dietary period ended. In the fasting state, the Med Diet consumption induced a lower gene expression of the p65 subunit of NF-?B compared with the SFA-rich diet (P = 0·019). The ingestion of the Med Diet induced a lower gene postprandial expression of p65 (P = 0·033), MCP-1 (P = 0·0229) and MMP-9 (P = 0·041) compared with the SFA-rich diet, and a lower gene postprandial expression of p65 (P = 0·027) and TNF-? (P = 0·047) compared with the CHO-PUFA diet. Direct plasma quantification mostly reproduced the findings. Our data suggest that consumption of a Med Diet reduces the postprandial inflammatory response in mononuclear cells compared with the SFA-rich and CHO-PUFA diets in elderly people. These findings may be partly responsible for the lower CVD risk found in populations with a high adherence to the Med Diet.
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Mediterranean diet supplemented with coenzyme Q10 modifies the expression of proinflammatory and endoplasmic reticulum stress-related genes in elderly men and women.
J. Gerontol. A Biol. Sci. Med. Sci.
PUBLISHED: 10-20-2011
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We have investigated whether the quality of dietary fat and supplementation with coenzyme Q(10) (CoQ) modifies expression of genes related with inflammatory response and endoplasmic reticulum stress in elderly persons. Twenty participants received three diets for 4 weeks each: Mediterranean diet + CoQ (Med + CoQ), Mediterranean diet (Med), and saturated fatty acid-rich diet (SFA). After 12-hour fast, volunteers consumed a breakfast with a fat composition similar to that consumed in each of the diets. Med and Med + CoQ diets produced a lower fasting calreticulin, IL-1b, and JNK-1 gene expression; a lower postprandial p65, IKK-b, MMP-9, IL-1b, JNK-1, sXBP-1, and BiP/Grp78 gene expression; and a higher postprandial IkB-a gene expression compared with the SFA diet. Med + CoQ diet produced a lower postprandial decrease p65 and IKK-b gene expression compared with the other diets. Our results support the anti-inflammatory effect of Med diet and that exogenous CoQ supplementation in synergy with a Med diet modulates the inflammatory response and endoplasmic reticulum stress.
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NOS3 Glu298Asp polymorphism interacts with virgin olive oil phenols to determine the postprandial endothelial function in patients with the metabolic syndrome.
J. Clin. Endocrinol. Metab.
PUBLISHED: 08-03-2011
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Glu298Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene (NOS3) has been characterized as a risk factor of hypertension and coronary artery disease. Previous studies suggest that the higher risk observed in T allele carriers is due to endothelial dysfunction associated with a lower eNOS activity and that acute consumption of phenol-rich olive oil ameliorates postprandial endothelial dysfunction by reducing oxidative stress and increasing nitric oxide bioavailability. Nevertheless, how these facts may interact in a population with altered endothelial function such as metabolic syndrome patients remains unknown.
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Metabolic syndrome: evidences for a personalized nutrition.
Mol Nutr Food Res
PUBLISHED: 07-29-2011
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Both insulin resistance and dyslipidaemia are determined by genetic and environmental factors. Depending on their expression and their function, gene variants may influence either insulin action or other metabolic traits. Nutrition also plays an important role in the development and progression of these conditions. Genetic background may interact with habitual dietary fat composition, affecting predisposition to insulin resistance syndrome and individual responsiveness to changes in dietary fat intake. In this context, nutrigenetics has emerged as a multidisciplinary field focusing on studying the interactions between nutritional and genetic factors and health outcomes. Due to the complex nature of gene-environment interactions, however, dietary therapy may require a "personalized" nutrition approach in the future. Although the results have not always been consistent, gene variants that affect primary insulin action, and particularly their interaction with the environment, are important modulators of glucose metabolism. The purpose of this review is to present some evidence of studies that have already demonstrated the significance of gene-nutrient interactions (adiponectin gene, Calpain-10, glucokinase regulatory protein, transcription factor 7-like 2, leptin receptor, scavenger receptor class B type I etc.) that influence insulin resistance in subjects with metabolic syndrome.
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Nutrigenetics of the lipoprotein metabolism.
Mol Nutr Food Res
PUBLISHED: 07-27-2011
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It is well known that lipid metabolism is a cornerstone in the development of the commonest important chronic diseases worldwide, such as obesity, cardiovascular disease, or metabolic syndrome. In this regard, the area of lipid and lipoprotein metabolism is one of the areas in which the understanding of the development and progression of those metabolic disorders has been studied in greater depth. Thus, growing evidence has demonstrated that while universal recommendations might be appropriate for the general population, in this area there is great variability among individuals, related to a combination of environmental and genetic factors. Moreover, the interaction between genetic and dietary components has helped in understanding this variability. Therefore, with further study into the interaction between the most important genetic markers or single-nucleotide polymorphisms (SNPs) and diet, it may be possible to understand the variability in lipid metabolism, which could lead to an increase in the use of personalized nutrition as the best support to combat metabolic disorders. This review discusses some of the evidence in which candidate SNPs can affect the key players of lipid metabolism and how their phenotypic manifestations can be modified by dietary intake.
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Postprandial antioxidant gene expression is modified by Mediterranean diet supplemented with coenzyme Q(10) in elderly men and women.
Age (Dordr)
PUBLISHED: 07-06-2011
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Postprandial oxidative stress is characterized by an increased susceptibility of the organism towards oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. We have investigated whether the quality of dietary fat alters postprandial gene expression and protein levels involved in oxidative stress and whether the supplementation with coenzyme Q(10) (CoQ) improves this situation in an elderly population. Twenty participants were randomized to receive three isocaloric diets each for 4 weeks: Mediterranean diet supplemented with CoQ (Med?+?CoQ diet), Mediterranean diet (Med diet), saturated fatty acid-rich diet (SFA diet). After 12-h fast, volunteers consumed a breakfast with a fat composition similar to that consumed in each of the diets. Nrf2, p22(phox) and p47(phox), superoxide dismutase 1 and 2 (SOD1 and SOD2), glutathione peroxidase 1 (GPx1), thiorredoxin reductase (TrxR) gene expression and Kelch-like ECH associating protein 1 (Keap-1) and citoplasmic and nuclear Nrf2 protein levels were determined. Med and Med?+?CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet. Moreover, Med?+?CoQ diet produced lower postprandial Nrf2 gene expression and lower nuclear Nrf2 protein levels compared to the other diets and lower GPx1 gene expression than the SFA diet. Our results support the antioxidant effect of a Med diet and that exogenous CoQ supplementation has a protective effects against free radical overgeneration through the lowering of postprandial oxidative stress modifying the postprandial antioxidant protein levels and reducing the postprandial expression of antioxidant genes in peripheral blood mononuclear cells.
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A variant near the melanocortin-4 receptor gene regulates postprandial lipid metabolism in a healthy Caucasian population.
Br. J. Nutr.
PUBLISHED: 06-07-2011
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The melanocortin-4 receptor (MC4R) is an essential regulator of food intake and energy homeostasis. Previous data suggest an influence of MC4R activity on TAG levels. Thus, the aim of the present study was to determine whether the presence of the rs12970134 polymorphism near the MC4R gene could influence postprandial lipoprotein metabolism in healthy subjects. A total of eighty-eight volunteers were selected, fifty-three homozygous for the common genotype (G/G) and thirty-five carriers for the minor A-allele (G/A and A/A). They were given a fat-rich meal containing 1 g fat and 7 mg cholesterol/kg body weight and vitamin A (60,000 IU/m(2) body surface). Fat accounted for 60 % of energy, and protein and carbohydrates accounted for 15 and 25 % of energy, respectively. Blood samples were taken at time 0, every 1 h until 6 h and every 2·5 h until 11 h. Total cholesterol and TAG in plasma, and cholesterol, TAG and retinyl palmitate in TAG-rich lipoproteins (TRL, large and small TRL) were separated by ultracentrifugation. Individuals carrying the G/G genotype displayed a higher postprandial response of plasma TAG (P = 0·033), total cholesterol (P = 0·019) and large TRL-TAG (P = 0·023) than did carriers of the minor A-allele. Furthermore, G/G subjects showed a greater postprandial response of small TRL-apoB48 than did carriers of the A-allele (P = 0·032). These results suggest that the rs12970134 polymorphism near the MC4R gene region may partly explain the inter-individual differences in postprandial lipoprotein response in healthy subjects.
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Clinical characteristics and evaluation of LDL-cholesterol treatment of the Spanish Familial Hypercholesterolemia Longitudinal Cohort Study (SAFEHEART).
Lipids Health Dis
PUBLISHED: 05-12-2011
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Familial hypercholesterolemia (FH) patients are at high risk for premature coronary heart disease (CHD). Despite the use of statins, most patients do not achieve an optimal LDL-cholesterol goal. The aims of this study are to describe baseline characteristics and to evaluate Lipid Lowering Therapy (LLT) in FH patients recruited in SAFEHEART.
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Mediterranean diet reduces senescence-associated stress in endothelial cells.
Age (Dordr)
PUBLISHED: 03-25-2011
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This paper aims to study the effects of the oxidative stress induced by quality and quantity of dietary fat on cellular senescence. Twenty elderly subjects consumed three diets, each for 4 weeks: a saturated fatty acid diet (SFA), a low-fat and high-carbohydrate diet (CHO-ALA), and a Mediterranean diet (MedDiet) enriched in monounsaturated fatty acid following a randomized crossover design. For each diet, we investigated intracellular reactive oxidative species (ROS), cellular apoptosis and telomere length in human umbilical endothelial cells incubated with serum from each patient. MedDiet induced lower intracellular ROS production, cellular apoptosis, and percentage of cell with telomere shortening, compared with the baseline and with SFA and CHO-ALA diets. Dietary fat modulates the oxidative stress in human endothelial cells. MedDiet protects these cells from oxidative stress, prevents cellular senescence and reduces cellular apoptosis.
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[Dietary fats and cardiovascular health].
Aten Primaria
PUBLISHED: 03-12-2011
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Although dietary fat and its role in cardiovascular prevention has been one of the most extensively studied nutritional topics, it continues to be an ever-expanding research area. Particularly thanks to studies on Mediterranean diet, we now know that fat quality is more relevant than the amount of fat we eat in the diet. Thus, saturated and trans fats have been found to increase the risk of atherogenic disease. This is why it is recommended to substitute complex carbohydrates or unsaturated fat for unsaturated and trans fats with the aim of reducing saturated and trans fat intake to <10% and <1%, respectively, of the total calorie intake. Recent population studies, particularly that conducted in Kuopio, Finland, and those on Mediterranean diet, stress the important role of monounsaturated and polyunsaturated fats as key nutrients in preventing cardiovascular disease in modern societies. Furthermore, a special type of polyunsaturated fatty acids, i.e. those of the omega-3 (n-3) series, is increasingly becoming essential nutrients for a healthy diet, especially in the case of children. Therefore, there is a rationale for four the Scientific Societies that are strongly committed to disseminate the benefits of a healthy diet in preventing cardiovascular disease, and to prepare a joint statement with the purpose of spreading improved knowledge on the importance of changing to a healthy diet with a well-balanced fat intake for industrialized populations. Accordingly, a multidisciplinary panel of experts from the following institutions has developed the present joint statement targeted at both adults and children of different ages: Spanish Society of Arteriosclerosis, Spanish Society of Family and Community Medicine, Spanish Association of Paediatrics, Spanish Society of Gastroenterology, Hepatology and Paediatric Nutrition and Dietetics, and Spanish Society for Food Sciences.
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R353Q polymorphism in the factor VII gene and cardiovascular risk in Heterozygous Familial Hypercholesterolemia: a case-control study.
Lipids Health Dis
PUBLISHED: 02-27-2011
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Heterozygous Familial Hypercholesterolemia (FH) is a genetic disorder characterized by a high risk of cardiovascular disease. Certain polymorphisms of the factor VII gene have been associated with the development of coronary artery disease and there is a known association between factor VII levels and polymorphic variants in this gene. To date, no study has evaluated the association between factor VII and coronary artery disease in patients with FH.
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Interleukin 1B variant -1473G/C (rs1143623) influences triglyceride and interleukin 6 metabolism.
J. Clin. Endocrinol. Metab.
PUBLISHED: 02-09-2011
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IL1b (IL1B or IL1?), a key modulator of the immune response, exerts its functions mainly via IL6 regulation. Fatty meals cause transient hypertriglyceridemia and are considered to be proinflammatory, but the extent of these responses shows high interindividual susceptibility.
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Dietary oil modifies the plasma proteome during aging in the rat.
Age (Dordr)
PUBLISHED: 01-30-2011
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Fatty acids and other components of the diet may modulate, among others, mechanisms involved in homeostasis, aging, and age-related diseases. Using a proteomic approach, we have studied how dietary oil affected plasma proteins in young (6 months) or old (24 months) rats fed lifelong with two experimental diets enriched in either sunflower or virgin olive oil. After the depletion of the most abundant proteins, levels of less abundant proteins were studied using two-dimensional electrophoresis and mass spectrometry. Our results showed that compared with the sunflower oil diet, the virgin olive oil diet induced significant decreases of plasma levels of acute phase proteins such as inter-alpha inhibitor H4P heavy chain (at 6 months), hemopexin precursor (at 6 and 24 months), preprohaptoglobin precursor (at 6 and 24 months), and ?-2-HS glycoprotein (at 6 and 24 months); antioxidant proteins such as type II peroxiredoxin (at 24 months); proteins related with coagulation such as fibrinogen ?-chain precursor (at 24 months), T-kininogen 1 precursor (at 6 and 24 months), and apolipoprotein H (at 6 and 24 months); or with lipid metabolism and transport such as apolipoprotein E (at 6 and 24 months) and apolipoprotein A-IV (at 24 months). The same diet increased the levels of apolipoprotein A-1 (at 6 and 24 months), diminishing in general the changes that occurred with age. Our unbiased analysis reinforces the beneficial role of a diet rich in virgin olive oil compared with a diet rich in sunflower oil, modulating inflammation, homeostasis, oxidative stress, and cardiovascular risk during aging.
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Olive oil and haemostasis: platelet function, thrombogenesis and fibrinolysis.
Curr. Pharm. Des.
PUBLISHED: 01-28-2011
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Mediterranean diet is one of the healthiest nutritional models used in developed countries. The actual interest in this dietary model is based in two main premises. First, the high palatability for the consumer, which aids to the adherence to the model on a life-long basis, and second, the mounting evidence on the beneficial properties that its consumption provokes in cardiovascular risk factors, cancer and cognitive age associated decline. Olive oil is the principal component of Mediterranean diet, both by its predominant position as the main energy source, and its presence in almost all cooked and/or seasoned food. The influence of the olive oil on the beneficial effects of the Mediterranean diet is well known. Albeit an initial stage in which monounsaturated fatty acids (mainly oleic acid) were studied as the sole player of these effects, the knowledge about the micronutrients has evolved to a much more complex model in which the processing of the oil and the content in some minor contents of the virgin olive oil play a fundamental role. In this article we will review the current evidences that relate olive oil with the haemostatic system.
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Mediterranean diet rich in olive oil and obesity, metabolic syndrome and diabetes mellitus.
Curr. Pharm. Des.
PUBLISHED: 01-28-2011
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After decades of epidemiological, clinical and experimental research, it has become clear that consumption of Mediterranean dietary patterns rich in olive oil has a profound influence on health outcomes, including obesity, metabolic syndrome (MetS) and diabetes mellitus. Traditionally, many beneficial properties associated with this oil have been ascribed to its high oleic acid content. Olive oil, however, is a functional food that, besides having high-monounsaturated (MUFA) content, contains other minor components with biological properties. In this line, phenolic compounds have shown antioxidant and antiinflammatory properties, prevent lipoperoxidation, induce favorable changes of lipid profile, improve endothelial function, and disclose antithrombotic properties. Research into the pharmacological properties of the minor components of olive oil is very active and could lead to the formulation of functional food and nutraceuticals. Although more data are mandatory the Mediterranean diet rich in olive oil does not contribute to obesity and appears to be a useful tool in the lifestyle management of the MetS. Moreover there is good scientific support for MUFA diets, especially those based on olive oil, as an alternative approach to low-fat diets for the medical nutritional therapy in diabetes. The objective of this review is to present evidence illustrating the relationship between Mediterranean diet, olive oil and metabolic diseases, including obesity, MetS and diabetes mellitus and to discuss potential mechanisms by which this food can help in disease prevention and treatment.
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Nutrigenetics of the postprandial lipoprotein metabolism: evidences from human intervention studies.
Curr Vasc Pharmacol
PUBLISHED: 01-14-2011
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Accumulating evidence suggests that elevated plasma triglycerides concentrations, in both the fasting and the postprandial states, may pose a significant independent risk for cardiovascular disease (CVD). Both fasting and postprandial lipoprotein concentrations vary substantially among individuals, and this inter individual variability is driven by a combination of non-genetic and genetic factors. Regarding the genetic component, the efforts to elucidate the variability in postprandial response have resulted in the identification of associations with multiple lipid candidate genes. However, most reported associations are based on very simple models including one single-nucleotide polymorphism (SNP) or haplotype at a time and small sample sizes. Progress in this promising area of research requires more comprehensive experimental models, including larger sample sizes that will allow investigating gene-gene interactions. Reviews of the literature in the area of ApoA5, GCKR, and PLIN genes and postprandial lipemia are used to demonstrate the complexities of genotype-phenotype associations. Knowledge of how these and other genes influence postprandial response should increase the understanding of personalised nutrition.
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Mediterranean diet supplemented with coenzyme Q10 induces postprandial changes in p53 in response to oxidative DNA damage in elderly subjects.
Age (Dordr)
PUBLISHED: 01-11-2011
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Coenzyme Q10 (CoQ) is a powerful antioxidant that reduces oxidative stress. We explored whether the quality of dietary fat alters postprandial oxidative DNA damage and whether supplementation with CoQ improves antioxidant capacity by modifying the activation/stabilization of p53 in elderly subjects. In this crossover study, 20 subjects were randomly assigned to receive three isocaloric diets during 4 weeks each: (1) Mediterranean diet (Med diet), (2) Mediterranean diet supplemented with CoQ (Med+CoQ diet), and (3) saturated fatty acid-rich diet (SFA diet). Levels of mRNAs were determined for p53, p21, p53R2, and mdm2. Protein levels of p53, phosphorylated p53 (Ser20), and monoubiquitinated p53 were also measured, both in cytoplasm and nucleus. The extent of DNA damage was measured as plasma 8-OHdG. SFA diet displayed higher postprandial 8-OHdG concentrations, p53 mRNA and monoubiquitinated p53, and lower postprandial Mdm2 mRNA levels compared with Med and Med+CoQ diets (p?
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Mediterranean diet reduces endothelial damage and improves the regenerative capacity of endothelium.
Am. J. Clin. Nutr.
PUBLISHED: 12-01-2010
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Endothelial dysfunction is a fundamental step in the atherosclerotic disease process. Activation or injury of the endothelium leads to a variety of inflammatory disorders, including the release of microparticles. Endothelial progenitor cells may contribute to the maintenance of the endothelium by replacing injured mature endothelial cells.
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Fructose addition to a glucose supplement modifies perceived exertion during strength and endurance exercise.
J Strength Cond Res
PUBLISHED: 11-12-2010
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The addition of fructose (F) to a glucose (G) supplement may modify the metabolic response during exercise; however, its effect on perceived exertion (PE) and its influence on postprandial metabolism have not been jointly studied in different types of exercise. This study sought to assess the acute effects of F addition to a G supplement on PE and on the postprandial metabolic response during a single bout of either strength exercise (SE) or endurance exercise (EE). Twenty physically trained men ingested an oral dose of G or GF 15 minutes before starting a 30-minute session of SE (10 sets of 10 repetitions of half squat) or EE (cycling). The combination resulted in 4 randomized interventions in a crossover design in which all subjects performed all experimental conditions: G + SE, GF + SE, G + EE, and GF + SE. Perceived exertion, heart rate (HR), G, insulin, lactate, and urinary catecholamine levels were measured before exercise, during the exercise, and during acute recovery. Perceived exertion during exercise was lower for GF than for G during SE and EE (mean ± SD; 8.95 ± 0.62 vs. 9.26 ± 0.65, p < 0.05 and 7.47 ± 0.84 vs. 7.74 ± 0.93, p < 0.05, respectively). The glycemic peak in GF + SE was lower than in G + SE (p < 0.05), and there was a second peak during recovery (p < 0.05), whereas in EE, no difference in blood G levels was noted between G and GF supplements. Moreover, HR, urinary adrenalin, and noradrenalin were lower in GF than in G (p < 0.05), though only for EE. The results showed that PE is positively affected by GF supplementation for both SE and EE and thus may be a useful dietary strategy for helping to achieve higher training loads.
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A low-fat, high-complex carbohydrate diet supplemented with long-chain (n-3) fatty acids alters the postprandial lipoprotein profile in patients with metabolic syndrome.
J. Nutr.
PUBLISHED: 07-14-2010
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Dietary fat intake plays a critical role in the development of metabolic syndrome (MetS). This study addressed the hypothesis that dietary fat quantity and quality may differentially modulate postprandial lipoprotein metabolism in MetS patients. A multi-center, parallel, randomized, controlled trial conducted within the LIPGENE study randomly assigned MetS patients to 1 of 4 diets: high-SFA [HSFA; 38% energy (E) from fat, 16% E as SFA], high-monounsaturated fatty acid [HMUFA; 38% E from fat, 20% E as MUFA], and 2 low-fat, high-complex carbohydrate [LFHCC; 28% E from fat] diets supplemented with 1.24 g/d of long-chain (LC) (n-3) PUFA (ratio 1.4 eicosapentaenoic acid:1 docosahexaenoic acid) or placebo (1.24 g/d of high-oleic sunflower-seed oil) for 12 wk each. A fat challenge with the same fat composition as the diets was conducted pre- and postintervention. Postprandial total cholesterol, triglycerides (TG), apolipoprotein (apo) B, apo B-48, apo A-I, LDL-cholesterol, HDL-cholesterol and cholesterol, TG, retinyl palmitate, and apo B in TG-rich lipoproteins (TRL; large and small) were determined pre- and postintervention. Postintervention, postprandial TG (P < 0.001) and large TRL-TG (P = 0.009) clearance began earlier and was faster in the HMUFA group compared with the HSFA and LFHCC groups. The LFHCC (n-3) group had a lower postprandial TG concentration (P < 0.001) than the other diet groups. Consuming the LFHCC diet increased the TG (P = 0.04), large TRL-TG (P = 0.01), TRL-cholesterol (P < 0.001), TRL-retinyl palmitate (P = 0.001), and TRL-apo B (P = 0.002) area under the curve compared with preintervention values. In contrast, long-term ingestion of the LFHCC (n-3) diet did not augment postprandial TG and TRL metabolism. In conclusion, postprandial abnormalities associated with MetS can be attenuated with LFHCC (n-3) and HMUFA diets. The adverse postprandial TG-raising effects of long-term LFHCC diets may be avoided by concomitant LC (n-3) PUFA supplementation to weight-stable MetS patients.
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Postprandial antioxidant effect of the Mediterranean diet supplemented with coenzyme Q10 in elderly men and women.
Age (Dordr)
PUBLISHED: 07-02-2010
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Postprandial oxidative stress is characterized by an increased susceptibility of the organism towards oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. We have investigated whether the quality of dietary fat alters postprandial cellular oxidative stress and whether the supplementation with coenzyme Q(10) (CoQ) lowers postprandial oxidative stress in an elderly population. In this randomized crossover study, 20 participants were assigned to receive three isocaloric diets for periods of 4 week each: (1) Mediterranean diet supplemented with CoQ (Med+CoQ diet), (2) Mediterranean diet (Med diet), and (3) saturated fatty acid-rich diet (SFA diet). After a 12-h fast, the volunteers consumed a breakfast with a fat composition similar to that consumed in each of the diets. CoQ, lipid peroxides (LPO), oxidized low-density lipoprotein (oxLDL), protein carbonyl (PC), total nitrite, nitrotyrosine plasma levels, catalase, superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities and ischemic reactive hyperaemia (IRH) were determined. Med diet produced a lower postprandial GPx activity and a lower decrease in total nitrite level compared to the SFA diet. Med and Med+CoQ diets induced a higher postprandial increase in IRH and a lower postprandial LPO, oxLDL, and nitrotyrosine plasma levels than the SFA diet. Moreover, the Med+CoQ diet produced a lower postprandial decrease in total nitrite and a greater decrease in PC levels compared to the other two diets and lower SOD, CAT, and GPx activities than the SFA diet.In conclusion, Med diet reduces postprandial oxidative stress by reducing processes of cellular oxidation and increases the action of the antioxidant system in elderly persons and the administration of CoQ further improves this redox balance.
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Pre-exercise intake of different carbohydrates modifies ischemic reactive hyperemia after a session of anaerobic, but not after aerobic exercise.
J Strength Cond Res
PUBLISHED: 05-29-2010
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The acute ingestion of a supplement with different glycemic carbohydrates, including fructose, is a typical practice for athletes before exercising. Observational evidence suggests that different metabolic responses may modify the exercise-stimulated endothelium-dependent vasodilation. The purpose of the present study was to investigate whether endothelial reactivity, stimulated by anaerobic exercise (AnE) or aerobic exercise (AE), both performed with glycemic supplementation, is modified by the addition of fructose. Twenty physically trained men ingested an oral dose of glucose (G) or glucose plus fructose (F) 15 minutes before starting a 30-minute session of AnE (10 sets of 10 repetitions of half squat) or AE (cycling). The combination resulted in 4 randomized interventions in a crossover design in which all subjects performed all experimental conditions: G+AnE, F+AnE, G+AE, and F+AE. Ischemic reactive hyperemia (IRH), glycemia, plasma lipoperoxides (LPOs), nitric oxide (NO), and lactate were determined at baseline, exercise, and acute recovery time points. Immediately after AnE, IRH was 26.35% higher in F+AnE than in G+AnE (p<0.05); this difference rose to 27.24% at the end of the recovery period (p<0.05). The glycemic peak in F+AnE was lower than in G+AnE (p<0.05), and there was a second peak during recovery (p<0.05). There were no differences observed in LPO between anaerobic trials, but the NO bioavailability increased and was higher in F + AnE than in G+AnE after exercise and recovery (p<0.05). Residual lactate was also higher under the F+AnE condition (p<0.05). During AE, there were no differences in IRH, glycemia, or NO between groups, but LPO was significantly higher after F supplementation. These results suggest that the addition of fructose to a single G supplement ingested before a glycolitic exercise can modify the glucoregulation and increases ischemic reactive hyperemia.
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The insulin sensitivity response is determined by the interaction between the G972R polymorphism of the insulin receptor substrate 1 gene and dietary fat.
Mol Nutr Food Res
PUBLISHED: 05-22-2010
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Insulin resistance, a condition associated with type 2 diabetes mellitus, results from the interaction of environmental and genetic factors. The aim of this study was to explore the influence of the G972R polymorphism at the insulin receptor substrate 1 gene on insulin sensitivity in a healthy young population. Furthermore, we examined whether the presence of this single nucleotide polymorphism (SNP; GR or GG) interacts with dietary fat to modulate insulin sensitivity.
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Gene variations of nitric oxide synthase regulate the effects of a saturated fat rich meal on endothelial function.
Clin Nutr
PUBLISHED: 04-29-2010
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Endothelial nitric oxide synthase (eNOS) gene variations have been linked to a higher risk for cardiovascular diseases (CVD) by unknown mechanisms. Our aim was to determine if two single nucleotide polymorphisms (SNPs) located in NOS3 (E298D and i19342) interfere with microvascular endothelial function (MEF) and/or oxidative stress during the postprandial state.
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Postprandial oxidative stress is modified by dietary fat: evidence from a human intervention study.
Clin. Sci.
PUBLISHED: 04-28-2010
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Previous evidence supports the concept that increased oxidative stress may play an important role in MetS (metabolic syndrome)-related manifestations. Dietary fat quality has been proposed to be critical in oxidative stress and the pathogenesis of the MetS. In the present study, we investigated whether oxidative stress parameters are affected by diets with different fat quantity and quality during the postprandial state in subjects with the MetS. Patients were randomly assigned to one of four isoenergetic diets distinct in fat quantity and quality for 12 weeks: a high-saturated-fatty-acid (HSFA) diet, a high-mono-unsaturated-fatty-acid (HMUFA) diet and two low-fat/high-complex carbohydrate diets [supplemented with 1.24 g/day of long-chain n-3 polyunsaturated fatty acid (LFHCC n-3) or with 1 g/day of sunflower oil high in oleic acid (LFHCC) as placebo]. The HMUFA diet enhanced postprandial GSH (reduced glutathione) levels and the GSH/GSSH (oxidized glutathione) ratio, compared with the other three diets. In addition, after the HMUFA-rich diet postprandial lipid peroxide levels, protein carbonyl concentrations, SOD (superoxide dismutase) activity and plasma H2O2 levels were lower compared with subjects adhering to the HSFA-rich diet. Both LFHCC diets had an intermediate effect relative to the HMUFA and HSFA diets. In conclusion, our data support the notion that the HMUFA diet improves postprandial oxidative stress in patients with the MetS. These findings suggest that the postprandial state is important for understanding the possible cardioprotective effects associated with mono-unsaturated dietary fat, particularly in subjects with the MetS.
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Gene expression changes in mononuclear cells in patients with metabolic syndrome after acute intake of phenol-rich virgin olive oil.
BMC Genomics
PUBLISHED: 04-20-2010
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Previous studies have shown that acute intake of high-phenol virgin olive oil reduces pro-inflammatory, pro-oxidant and pro-thrombotic markers compared with low phenols virgin olive oil, but it still remains unclear whether effects attributed to its phenolic fraction are exerted at transcriptional level in vivo. To achieve this goal, we aimed at identifying expression changes in genes which could be mediated by virgin olive oil phenol compounds in the human.
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ABCA1 gene variants regulate postprandial lipid metabolism in healthy men.
Arterioscler. Thromb. Vasc. Biol.
PUBLISHED: 02-25-2010
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Genetic variants of ABCA1, an ATP-binding cassette (ABC) transporter, have been linked to altered atherosclerosis progression and fasting lipid concentration, mainly high-density lipoproteins and apolipoprotein A1; however, results from different studies have been inconsistent.
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Update on genetics of postprandial lipemia.
Atheroscler Suppl
PUBLISHED: 02-23-2010
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The relationship between alimentary lipemia and coronary disease is of great interest in view of the epidemiological and experimental evidence that underlies it. The modulation of such phenomena is influenced by both genetic and environmental factors, thus explaining their extraordinary individual variance. Over the last two decades there has been an explosion of research in this area, with often conflicting findings reported in the literature. In this study we have presented the current evidence linking a number of candidate genes (APOA1/C3/A4/A5 cluster, ABCA1, CETP, GCKR, HL, IL-6, LPL, PLIN, and TCF7L2) to the modulation of the postprandial lipid metabolism. Increased knowledge of how these and other genes influence postprandial response should increase the understanding of personalised nutrition.
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APOA1 and APOA4 gene polymorphisms influence the effects of dietary fat on LDL particle size and oxidation in healthy young adults.
J. Nutr.
PUBLISHED: 02-17-2010
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We investigated whether APOA1 and APOA4 genotypes interact with diet to determine changes in LDL size and their susceptibility to oxidative modifications. A total of 97 healthy volunteers each consumed 3 diets for 4 wk: a SFA diet (38% fat, 20% SFA) followed by a low-fat and high-carbohydrate (CHO) diet (30% fat, 55% carbohydrate) or a monounsaturated fatty acid (MUFA) diet (38% fat, 22% MUFA) following a randomized crossover design. For each diet, we determined susceptibility to oxidative modifications and LDL size. To investigate the combined effects of the APOA1 G-76A and APOA4 Thr347Ser single nucleotide polymorphisms (SNP), we defined 4 combined genotype groups: GG/ThrThr, GG/ThrSer, GA/ThrThr, and GA/ThrSer. After participants consumed the CHO diet, there was a significant decrease in LDL size with respect to high-fat diets in GG homozygotes for the APOA1 G-76A SNP. However, LDL size did not differ in GA carriers among participants consuming the 3 diets. Carriers of the A allele for this polymorphism had smaller LDL size as well as increased susceptibility to oxidation after the SFA diet than the GG homozygous. Moreover, the interaction between the APO A1 and APOA4 genotypes revealed that individuals with the GA/ThrSer genotype had larger LDL particle size during consumption of the MUFA diet than when they consumed the CHO diet. No differences in LDL oxidation were found in this analysis. Our study supports the concept that SNP in APOA1and APOA4 genes influences atherogenic characteristics of LDL particles in response to diet.
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A dose of fructose induces oxidative stress during endurance and strength exercise.
J Sports Sci
PUBLISHED: 09-19-2009
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This study sought to compare the time course changes in oxidative state and glycemic behavior when glucose or glucose plus fructose are consumed before endurance and strength exercise. After two weeks on a controlled diet, 20 physically trained males ingested an oral dose of glucose or glucose plus fructose, 15 min before starting a moderate-intensity 30-min session of endurance or strength exercise. The combination resulted in four randomized interventions: glucose or glucose plus fructose + endurance exercise and glucose or glucose plus fructose + strength exercise, which were implemented consecutively in random order at 1-week intervals. Plasma concentration of lipoperoxides, oxidized LDL, reduced glutathione, catalase and glycemia were determined at baseline, during exercise and acute recovery. Following the ingestion of glucose plus fructose, lipoperoxides, catalase and reduced glutathione depletion were significantly higher than following consumption of glucose, for both endurance and strength exercise (P < 0.05). Oxidized LDL-c was higher after glucose plus fructose than after glucose alone in endurance exercise (P < 0.05). There was no difference in the glycemic peak between glucose plus fructose and glucose ingestion in endurance exercise trials. In strength exercise, the post-absorptive glycemic peak was less when the participants ingested glucose plus fructose than glucose (P < 0.05), and a second peak was found in the recovery phase of this group (P < 0.05). In conclusion, the addition of fructose to a pre-exercise glucose supplement triggers oxidative stress.
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The effect of apoE genotype and sex on ApoE plasma concentration is determined by dietary fat in healthy subjects.
Br. J. Nutr.
PUBLISHED: 09-04-2009
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The interindividual variation in ApoE plasma concentration is considerable, mainly determined by apoE genotype and sex. However, a large amount of variability remains unexplained by these factors. We have evaluated whether the quantity and quality of dietary fat interacts with the apoE genotype and sex modifying ApoE plasma levels in young healthy subjects. Eighty-four volunteers (sixty-six apoE3/3, eight apoE4/3 and ten apoE3/2) were subjected to three dietary periods, each lasting 4 weeks. The first was a SFA-enriched diet (38 % fat and 20 % SFA), which was followed by a carbohydrate (CHO)-rich diet (30 % fat, < 10 % SFA and 55 % carbohydrate) or a MUFA-rich diet (38 % fat and 22 % MUFA) following a randomised crossover design. apoE2 carriers have the highest ApoE levels, whereas apoE4 individuals show the lowest concentration after the SFA, CHO and MUFA diets. Women had significantly higher ApoE concentration than men only after the consumption of the SFA diet. The SFA diet increased the ApoE plasma concentration when compared with the CHO- and MUFA-rich diets in women, but not in men. In women, but not in men, the shift from the SFA- to CHO- or MUFA-rich diets significantly decreased the ApoE concentration in apoE3/2 and apoE3/3 subjects, whereas no differences were observed in women with the apoE4/3 genotype. Sex and apoE genotype determine ApoE plasma levels; however, this effect is dependent on dietary fat.
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Olive oil and walnut breakfasts reduce the postprandial inflammatory response in mononuclear cells compared with a butter breakfast in healthy men.
Atherosclerosis
PUBLISHED: 08-11-2009
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Inflammation is crucial in all stages of atherosclerosis, and few studies have investigated the effect of dietary fat on markers of inflammation related to this disease during the postprandial period.
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Dietary fat differentially influences regulatory endothelial function during the postprandial state in patients with metabolic syndrome: from the LIPGENE study.
Atherosclerosis
PUBLISHED: 07-08-2009
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To investigate whether endothelium-dependent vasomotor function and plasma levels of cellular adhesion molecules are affected by diets with different fat quantity and quality during the postprandial state in subjects with the metabolic syndrome (MetS).
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n-3 PUFA and lipotoxicity.
Biochim. Biophys. Acta
PUBLISHED: 06-02-2009
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Excess lipid accumulation in nonadipose tissues may occur in the setting of high levels of plasma free fatty acids or triglycerides (TGs) in a process called "lipotoxicity". Evidence from human studies and animal models suggests that lipid accumulation in the heart, skeletal muscle, pancreas, and liver play an important role in the pathogenesis of heart failure, obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM). During the past few years, several studies have shown that n-3 polyunsaturated fatty acids (PUFA) have potentially cardioprotective effects, especially in high-risk patients with dyslipidemia, and might therefore be expected to be of benefit in T2DM. Moreover, new information has demonstrated the beneficial effects of consuming n-3 PUFA in preventing the complications of lipotoxicity. n-3 PUFA dietary intake thus had positive effects on fatty liver in patients with non-alcoholic fatty liver disease (NAFLD), with an improvement in liver echotexture and a significant regression of hepatic brightness, associated with improved liver hemodynamics. The n-3 PUFA also had beneficial effects on ectopic fat accumulation inside the heart, with stabilization of cardiac myocytes and antiarrhythmic effects. On the other hand, recent data from animal models suggest that oral dosing of eicosapentaenoic acid (EPA) could contribute to protect against beta-cell lipotoxicity. This review discusses the latest hypotheses regarding lipotoxicity, concentrating on the impact of the n-3 PUFA that contribute to ectopic lipid storage, affecting organ function. Further human studies are needed to test the evidence and elucidate the mechanisms involved in this process.
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[Clinical-ultrasonographic assessment in arthroscopic rotator cuff repair after 1-year follow-up].
Acta Ortop Mex
PUBLISHED: 05-26-2009
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Arthroscopic repair of the rotator cuff have shown have shown encouraging clinical results. However, few authors have assessed integrity of repair with ultrasound. The presence of re-rupture by ultrasonography in a rotator cuff repair may not relate to the patients functional status.
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[Study of celiac disease in adults with type 1 diabetes mellitus].
Gastroenterol Hepatol
PUBLISHED: 05-18-2009
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Celiac disease (CD) presents a wide clinical spectrum. There are asymptomatic or oligosymptomatic forms, which are difficult to diagnose. Since patients with untreated CD can develop severe complications, early diagnosis of these forms is important. Consequently, in groups at risk for CD, such as patients with type 1 diabetes (DM1), screening through determination of antigliadin (AGA), anti-tissue transglutaminase (ATG) and antiendomysial antibodies (EMA) is recommended. In the present study, 463 DM1 patients were screened for these antibodies. Patients who were positive for one or more were offered an upper endoscopy to obtain distal duodenum biopsies. Histological lesions, when present, were classified using Marshs classification. Of the 463 patients, 62 (13.4%) were positive for at least one of the three antibodies, and 42 accepted to undergo an endoscopy. Fourteen patients (3% of the DM1 patients) were histologically diagnosed with CD. Most of these patients had no symptoms of CD, although some showed laboratory findings frequent in CD. The presence of clinical or analytical data compatible with CD was independent of the grade of histological lesions. Finally, we calculated the sensitivity and positive predictive value for each antibody. The most sensitive were ATG and EMA. Because of the technical simplicity of determining ATG with ELISA, in our opinion, this test should be the option of choice for screening.
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[Results of arthroscopic debridement and lavage in patients with knee osteoarthritis].
Acta Ortop Mex
PUBLISHED: 05-13-2009
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Knee osteoarthritis (OA) is a degenerative process that affects people over 50 years old and is an important cause of disability. Treatment options include non-operative and operative modalities. Arthroscopic lavage and debridement may be the first choice to consider in patients between 45 and 65 years with early OA.
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[Cost analysis and economic impact of anterior cruciate ligament reconstruction].
Acta Ortop Mex
PUBLISHED: 04-20-2009
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Health economics studies play an important role in all healthcare systems. The purpose of the latter is to offer effective and low-cost treatments.
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Fructose modifies the hormonal response and modulates lipid metabolism during aerobic exercise after glucose supplementation.
Clin. Sci.
PUBLISHED: 02-21-2009
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The metabolic response when aerobic exercise is performed after the ingestion of glucose plus fructose is unclear. In the present study, we administered two beverages containing GluF (glucose+fructose) or Glu (glucose alone) in a randomized cross-over design to 20 healthy aerobically trained volunteers to compare the hormonal and lipid responses provoked during aerobic exercise and the recovery phase. After ingesting the beverages and a 15-min resting period, volunteers performed 30 min of moderate aerobic exercise. Urinary and blood samples were taken at baseline (t(-15)), during the exercise (t(0), t(15) and t(30)) and during the recovery phase (t(45), t(75) and t(105)). Plasma insulin concentrations were higher halfway through the exercise period and during acute recuperation (t(15) and t(75); P<0.05) following ingestion of GluF than after Glu alone, without any differences between the effects of either intervention on plasma glucose concentrations. Towards the end of the exercise period, urinary catecholamine concentrations were lower following GluF (t(45); P<0.05). Plasma triacylglycerol (triglyceride) concentrations were higher after the ingestion of GluF compared with Glu (t(15), t(30), t(45) and t(105); P<0.05). Furthermore, with GluF, we observed higher levels of lipoperoxides (t(15), t(30), t(45) and t(105); P<0.05) and oxidized LDL (low-density lipoprotein; t(30); P<0.05) compared with after the ingestion of Glu alone. In conclusion, hormonal and lipid alterations are provoked during aerobic exercise and recovery by the addition of a dose of fructose to the pre-exercise ingestion of glucose.
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