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Find video protocols related to scientific articles indexed in Pubmed.
Genome-wide association study of liver enzymes in korean children.
Genomics Inform
PUBLISHED: 07-31-2013
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Liver enzyme elevations, as an indicator of liver function, are widely associated with metabolic diseases. Genome-wide population-based association studies have identified a genetic susceptibility to liver enzyme elevations and their related traits; however, the genetic architecture in childhood remains largely unknown. We performed a genome-wide association study to identify new genetic loci for liver enzyme levels in a Korean childhood cohort (n = 484). We observed three novel loci (rs4949718, rs80311637, and rs596406) that were multiply associated with elevated levels of alanine transaminase and aspartate transaminase. Although there are some limitations, including genetic power, additional replication and functional characterization will support the clarity on the genetic contribution that the ST6GALNAC3, ADAMTS9, and CELF2 genes have in childhood liver function.
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Piperine reverses high fat diet-induced hepatic steatosis and insulin resistance in mice.
Food Chem
PUBLISHED: 05-22-2013
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This study examined the effect of piperine on hepatic steatosis and insulin resistance induced in mice by feeding a high-fat diet (HFD) for 13 weeks and elucidated potential underlying molecular mechanisms. Administration of piperine (50 mg/kg body weight) to mice with HFD-induced hepatic steatosis resulted in a significant increase in plasma adiponectin levels. Also, elevated plasma concentrations of insulin and glucose and hepatic lipid levels induced by feeding a HFD were reversed in mice when they were administered piperine. However, piperine did not reduce body weight and other biochemical markers to an extent where they became equal to the levels found in the CD-fed mice. Piperine reversed HFD-induced down-regulation of adiponecitn-AMP-activated protein kinase (AMPK) signalling molecules which play an important role in mediating lipogenesis, fatty acid oxidation and insulin signalling in the livers of mice. The expressions of lipogenic target genes were decreased, whereas the expression of carnitine palmitoyltransferase 1 (CPT1) gene involved in fatty acid oxidation was increased in the livers of the Pin50 group. Piperine significantly decreased the phosphorylation of insulin receptor substrate-1 (IRS-1) compared with the HFD-fed mice. Administration of piperine appeared to reverse preexisting HFD-induced hepatic steatosis and insulin resistance, probably by activation of adiponectin-AMPK signalling in mice.
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Dietary camphene attenuates hepatic steatosis and insulin resistance in mice.
Obesity (Silver Spring)
PUBLISHED: 05-18-2013
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The aim of this study was to investigate the protective effects of camphene on high-fat diet (HFD)-induced hepatic steatosis and insulin resistance in mice and to elucidate its mechanism of action.
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Involvement of SIRT1-AMPK signaling in the protective action of indole-3-carbinol against hepatic steatosis in mice fed a high-fat diet.
J. Nutr. Biochem.
PUBLISHED: 01-18-2013
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This study addressed the effect of indole-3-carbinol (I3C) supplementation on hepatic steatosis in mice fed a high-fat diet (HFD) and clarified the underlying mechanism. Male C57BL/6N mice were divided into three groups: those who received a normal diet, those fed with HFD and those fed with 0.1% I3C-supplemented diet (I3CD). In the present study, an HFD supplemented with 0.1% I3C significantly decreased body and liver weight as well as plasma and hepatic lipid levels. The activation of the silent mating type information regulation 2 homolog 1 (SIRT1)-AMP-activated protein kinase (AMPK) signaling system by I3C correlated with decreased mRNA levels of sterol regulatory element-binding protein-1c-regulated lipogenic enzymes. In addition, I3C significantly reversed HFD-induced up-regulation of ER stress-mediated signaling molecules in the liver, which may have contributed to the protective effects of I3C against hepatic steatosis. Furthermore, HFD-induced up-regulations of inflammatory genes such as tumor necrosis factor ? and interleukin 6 were significantly reversed by dietary I3C supplementation. Our study suggests that the protective action of I3C against hepatic steatosis is mediated, at least in part, through the up-regulation of a SIRT1-AMPK signaling system in the livers of HFD-fed mice. Further investigations revealed that alleviation of the ER stress response represented a critical mechanism underlying the beneficial effects of I3C on hepatic steatosis.
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Induction of olfaction and cancer-related genes in mice fed a high-fat diet as assessed through the mode-of-action by network identification analysis.
PLoS ONE
PUBLISHED: 01-15-2013
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The pathophysiological mechanisms underlying the development of obesity and metabolic diseases are not well understood. To gain more insight into the genetic mediators associated with the onset and progression of diet-induced obesity and metabolic diseases, we studied the molecular changes in response to a high-fat diet (HFD) by using a mode-of-action by network identification (MNI) analysis. Oligo DNA microarray analysis was performed on visceral and subcutaneous adipose tissues and muscles of male C57BL/6N mice fed a normal diet or HFD for 2, 4, 8, and 12 weeks. Each of these data was queried against the MNI algorithm, and the lists of top 5 highly ranked genes and gene ontology (GO)-annotated pathways that were significantly overrepresented among the 100 highest ranked genes at each time point in the 3 different tissues of mice fed the HFD were considered in the present study. The 40 highest ranked genes identified by MNI analysis at each time point in the different tissues of mice with diet-induced obesity were subjected to clustering based on their temporal patterns. On the basis of the above-mentioned results, we investigated the sequential induction of distinct olfactory receptors and the stimulation of cancer-related genes during the development of obesity in both adipose tissues and muscles. The top 5 genes recognized using the MNI analysis at each time point and gene cluster identified based on their temporal patterns in the peripheral tissues of mice provided novel and often surprising insights into the potential genetic mediators for obesity progression.
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Carvacrol Protects against Hepatic Steatosis in Mice Fed a High-Fat Diet by Enhancing SIRT1-AMPK Signaling.
Evid Based Complement Alternat Med
PUBLISHED: 01-10-2013
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We investigated the protective effect of carvacrol against high-fat-diet-induced hepatic steatosis in mice and the potential underlying molecular mechanisms. Mice were fed a normal diet, high-fat diet, or carvacrol-supplemented high-fat diet for 10 weeks. Compared to mice fed the high-fat diet, those fed the carvacrol-supplemented diet showed significantly lower hepatic lipid levels and reduced plasma activities of alanine aminotransferase and aspartate aminotransferase and plasma concentrations of monocyte chemoattractant protein 1 and tumor necrosis factor ? . Carvacrol decreased the expression of LXR ? , SREBP1c, FAS, leptin, and CD36 genes and phosphorylation of S6 kinase 1 protein involved in lipogenesis, whereas it increased the expression of SIRT1 and CPT1 genes and phosphorylation of liver kinase B1, AMP-activated protein kinase, and acetyl-CoA carboxylase proteins involved in fatty acid oxidation in the liver of mice fed the high-fat diet. These results suggest that carvacrol prevents HFD-induced hepatic steatosis by activating SIRT1-AMPK signaling.
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Antilipogenic and anti-inflammatory activities of Codonopsis lanceolata in mice hepatic tissues after chronic ethanol feeding.
J. Biomed. Biotechnol.
PUBLISHED: 07-13-2011
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This study evaluated the antilipogenic and anti-inflammatory effects of Codonopsis lanceolata (C. lanceolata) root extract in mice with alcohol-induced fatty liver and elucidated its underlying molecular mechanisms. Ethanol was introduced into the liquid diet by mixing it with distilled water at 5% (wt/v), providing 36% of the energy, for nine weeks. Among the three different fractions prepared from the C. lanceolata root, the C. lanceolata methanol extract (CME) exhibited the most remarkable attenuation of alcohol-induced fatty liver with respect to various parameters such as hepatic free fatty acid concentration, body weight loss, and hepatic accumulations of triglyceride and cholesterol. The hepatic gene and protein expression levels were analysed via RT-PCR and Western blotting, respectively. CME feeding significantly restored the ethanol-induced downregulation of the adiponectin receptor (adipoR) 1 and of adipoR2, along with their downstream molecules. Furthermore, the study data showed that CME feeding dramatically reversed ethanol-induced hepatic upregulation of toll-like receptor- (TLR-) mediated signaling cascade molecules. These results indicate that the beneficial effects of CME against alcoholic fatty livers of mice appear to be with adenosine- and adiponectin-mediated regulation of hepatic steatosis and TLR-mediated modulation of hepatic proinflammatory responses.
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Carvacrol prevents diet-induced obesity by modulating gene expressions involved in adipogenesis and inflammation in mice fed with high-fat diet.
J. Nutr. Biochem.
PUBLISHED: 03-29-2011
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Carvacrol (2-methyl-5-isopropylphenol) is a monoterpene phenolic constituent of the essential oil produced by numerous aromatic plants and spices. The main objective of this study was to investigate effects of carvacrol in mice fed with a high-fat diet (HFD), which is an important model of obesity, and to study the potential underlying mechanisms focusing on the gene expression involved in adipogenesis, thermogenesis and inflammation. Male C57BL/6N mice were divided in three groups: those who received a normal diet, those fed with HFD and those fed with 0.1% carvacrol-supplemented diet (CSD). Body weight, visceral fat-pads and biochemical parameters were determined. Adipose tissue genes and protein expression levels were also assessed through reverse transcription polymerase chain reaction and Western blot analyses. Mice fed with CSD exhibited significantly reduced body weight gain, visceral fat-pad weights and plasma lipid levels compared with mice fed with HFD. Furthermore, HFD-induced up-regulations of adipose tissue genes and protein associated with the signaling cascades that lead to adipogenesis and inflammation were significantly reversed by dietary carvacrol supplementation. In summary, the major novel finding in our experimental conditions is that carvacrol prevented obesity in HFD-fed mice by decreasing body weight, visceral fat-pad weights and lowering plasma lipid levels. The evidence obtained in this study suggests that carvacrol appears to inhibit visceral adipogenesis probably by suppressing bone morphogenic protein-, fibroblast growth factor 1- and galanin-mediated signaling, and it also attenuates the production of pro-inflammatory cytokines in visceral adipose tissues by inhibiting toll like receptor 2 (TLR2)- and TLR4-mediated signaling.
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Obesity activates toll-like receptor-mediated proinflammatory signaling cascades in the adipose tissue of mice.
J. Nutr. Biochem.
PUBLISHED: 03-16-2011
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Obesity is characterized by low-grade and chronic inflammation, a phenomenon explained with a new term, metaflammation. Recent studies suggest that adipocytes may play an important role in the physiological regulation of immune responses in fat deposits via toll-like receptor (TLR) signaling cascades. This study investigates the role of the visceral as well as subcutaneous adipose tissues in the development of metaflammation by characterizing the tissue-specific expression profiles of TLRs and downstream signaling molecules and explores the differential responsiveness of TLR-mediated proinflammatory signaling cascades to diet-induced obesity (DIO) and obesity induced by a leptin gene deficiency. The obesity that was induced by a high-fat diet or leptin deficiency up-regulated the expression of TLR1-9 and TLR11-13 in murine adipose tissues, a phenomenon linked with downstream nuclear factor ?B, interferon regulatory factors, and STAT-1 activation, and up-regulated the expression of cytokines and chemokines via MyD88-dependent and MyD88-independent cascades. The extent of the obesity-induced up-regulation of most TLR genes and related proinflammatory signaling cascades was much greater in the epididymal adipose tissues than in the subcutaneous fat tissues of the mice with DIO. Furthermore, the magnitudes of the obesity-induced up-regulation of the TLR1, TLR4, TLR5, TLR8, TLR9, and TLR12 genes and most of the downstream signaling molecules and target cytokine genes in the visceral adipose tissue were greater in the DIO mice than in the ob/ob mice. These results suggest that TLRs and related proinflammatory signaling molecules that are overexpressed in enlarged adipose tissues may play an important role in the obesity-associated phenomenon of metaflammation.
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Resveratrol exerts anti-obesity effects via mechanisms involving down-regulation of adipogenic and inflammatory processes in mice.
Biochem. Pharmacol.
PUBLISHED: 03-09-2011
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Resveratrol is a natural polyphenolic stilbene derivative found in a variety of edible fruits, including nuts, berries, and grape skin. Although resveratrol has been suggested to improve thermogenesis in the brown adipose tissues of obese animals, there have been no reports on the anti-adipogenic and anti-inflammatory effects of resveratrol in the white adipose tissues of obese animals. The primary aim of this study was to investigate whether resveratrol attenuates high-fat diet (HFD)-induced adipogenesis and inflammation in the epididymal fat tissues of mice and to explore the underlying mechanisms involved in this attenuation. In comparison with HFD-fed mice, mice fed with a 0.4% resveratrol-supplemented diet (RSD) showed significantly lower body weight gain (-48%), visceral fat-pad weights (-58%), and plasma levels of triglyceride, FFA, total cholesterol, glucose, tumor necrosis factor (TNF) ?, and monocyte chemoattractant protein-1 (MCP1). Resveratrol significantly reversed the HFD-induced up-regulation of galanin-mediated signaling molecules (GalR1/2, PKC?, Cyc-D, E2F1, and p-ERK) and key adipogenic genes (PPAR?2, C/EBP?, SREBP-1c, FAS, LPL, aP2, and leptin) in the epididymal adipose tissues of mice. Furthermore, resveratrol significantly attenuated the HFD-induced up-regulation of pro-inflammatory cytokines (TNF?, IFN?, IFN?, and IL-6) and their upstream signaling molecules (TLR2/4, MyD88, Tirap, TRIF, TRAF6, IRF5, p-IRF3, and NF-?B) in the adipose tissues of mice. The results of this study suggest that resveratrol inhibits visceral adipogenesis by suppressing the galanin-mediated adipogenesis signaling cascade. It may also attenuate cytokine production in the adipose tissue by repressing the TLR2- and TLR4-mediated pro-inflammatory signaling cascades in HFD-fed mice.
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Hepatoprotective effect of oleuropein in mice: mechanisms uncovered by gene expression profiling.
Biotechnol J
PUBLISHED: 09-17-2010
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Oleuropein, an active constituent of olive leaf, has a variety of pharmacological activities associated with its capacity to scavenge reactive oxygen species. Oleuropein is also reported to have protective effects against non-alcoholic fatty liver disease (NAFLD) in vivo. In this study, gene expression profiling of hepatic tissues was examined, and transcription factors (TFs) with target genes that were modulated by oleuropein were identified to gain insights into the molecular mechanisms for the hepatoprotective action of this compound. C57BL/6N mice were fed either a high-fat diet (HFD) or 0.03% oleuropein-supplemented HFD for 10 weeks, after which their livers were subjected to oligo DNA microarray analysis. The oleuropein with which the HFD was supplemented reduced the hepatic mRNA level of the genes that encoded the key regulators of the hepatic fatty acid uptake and transport. In addition, the oleuropein reduced the expression of a number of hepatic genes involved in the oxidative stress responses and detoxification of lipid peroxidation products and proinflammatory cytokine genes. The (putative) candidate TFs that bound to the promoters of the genes regulated at least threefold (both up and down) by oleuropein were implicated in the lipogenesis, inflammation, insulin resistance, fibrosis, and cell proliferation and differentiation, which implies that the mechanisms that underlie the beneficial effects of oleuropein on NAFLD may be multifactorial.
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High-fat diet stimulates IL-1 type I receptor-mediated inflammatory signaling in the skeletal muscle of mice.
Mol Nutr Food Res
PUBLISHED: 02-19-2010
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Recently, substantial attention has been focused on the association between obesity and chronic inflammation. The aim of the present study was to investigate whether high-fat diet (HFD)-induced obesity induces the activation of the IL-1 type I receptor (IL-1RI)-mediated inflammatory signaling cascade in the skeletal muscle of mice. Male C57BL/6J mice were fed either an HFD or a normal diet (ND) for 12 wk. Compared with the results in mice receiving the ND, the HFD increased the expression of IL-1RI and downstream signaling proteins, such as myeloid differentiation primary response gene 88 (MyD88), IL-1R-associated kinase 4 and phospho-transforming growth factor-activated kinase 1 in the skeletal muscle. Additionally, activities of both inhibitor of kappaB kinase beta and inhibitor of kappaB degradation were significantly elevated in the skeletal muscle of mice fed with an HFD compared with mice receiving an ND. In contrast, the levels of other downstream transcription factors, such as activator protein-1 and INF regulatory factor 5, were not affected by the HFD. These results suggest that the IL-1RI-MyD88-nuclear factor kappaB signaling pathway might be involved in the induction of the inflammatory response in the skeletal muscle of mice fed with an HFD.
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Oleuropein attenuates hepatic steatosis induced by high-fat diet in mice.
J. Hepatol.
PUBLISHED: 01-09-2010
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Oleuropein, a secoiridoid derived from olives and olive oil, has been known to possess antimicrobial, antioxidative, and anticancer activities. The purpose of the present study was to determine whether oleuropein has a protective effect against hepatic steatosis induced by a high fat diet (HFD) and to elucidate its underlying molecular mechanisms in mice.
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Piperine, an LXR? antagonist, protects against hepatic steatosis and improves insulin signaling in mice fed a high-fat diet.
Biochem. Pharmacol.
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This study investigated the role of piperine in the transcriptional regulation of liver X receptor ? (LXR?) and the effects of dietary piperine on high-fat diet (HFD)-induced hepatic steatosis and insulin resistance in mice. Furthermore, we explored the potential molecular mechanisms through which the protective effects of piperine may work. In the present study, piperine significantly reduced ligand-induced LXR? activity in a dose-dependent manner and gradually disrupted the interaction between ligand-bound LXR? and GST-CBP. In mice, an HFD supplemented with 0.05% piperine (PSD) significantly decreased body and liver weight as well as plasma and hepatic lipid levels. In agreement with our in vitro study, in mice fed an HFD, dietary piperine markedly decreased LXR? mRNA expression and its lipogenic target genes (i.e., SREBP1c, ChREBP?, FAS, and CD36). Piperine also significantly decreased plasma insulin and glucose concentrations, while increasing insulin sensitivity in mice fed an HFD. In addition, piperine downregulated the expression of genes involved in ER stress, including GRP78, activating transcription factor 6, and eukaryotic translation initiation factor 2?, and upregulated GLUT2 translocation from the cytosol to the plasma membrane in the livers of PSD mice. Piperine antagonized LXR? transcriptional activity by abolishing the interaction of ligand-bound LXR? with the co-activator CBP. The effects of piperine on hepatic lipid accumulation were likely regulated via alterations in LXR?-mediated lipogenesis in mice fed an HFD. Dietary piperine also led to reduced ER stress and increased insulin sensitivity and prevented hepatic insulin resistance in mice fed the HFD.
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Indole-3-carbinol prevents diet-induced obesity through modulation of multiple genes related to adipogenesis, thermogenesis or inflammation in the visceral adipose tissue of mice.
J. Nutr. Biochem.
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Indole-3-carbinol (I3C) is a compound found in high concentrations in Brassica family vegetables, including broccoli, cauliflower and cabbage, and is regarded as a promising chemopreventive agent against various cancers. This study assesses the protective effect of I3C against diet-induced obesity in mice. Mice were randomly grouped to receive either a normal diet, high-fat (40% energy as fat) diet (HFD) or I3C-supplemented diet (1 g/kg diet) for 10 weeks. I3C supplementation significantly ameliorated HFD-induced increases in body weight gain, visceral fat pad weights and plasma lipid levels. The visceral adipose tissue mRNA levels of uncoupling proteins 1 and 3, crucial factors of thermogenesis, and their regulators such as sirtuin 1, peroxisome proliferator-activated receptor (PPAR) ? and PPAR? coactivator 1?, which were down-regulated by HFD, were normalized by supplementation with I3C. In contrast, I3C supplementation significantly decreased expression levels of a key adipogenic transcription factor, PPAR?2, and its target genes, such as leptin and adipocyte protein 2, in the visceral adipose tissue of mice maintained on the HFD. Furthermore, HFD-induced up-regulation in mRNA levels of inflammatory cytokines (tumor necrosis factor ?, interferon ? and interleukin 6) was significantly ameliorated by I3C. These findings suggest that I3C has a potential benefit in preventing obesity and metabolic disorders, and the action for I3C in vivo may involve multiple mechanisms including decreased adipogenesis and inflammation, along with activated thermogenesis.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.