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Find video protocols related to scientific articles indexed in Pubmed.
Initial experience with endoscopic sleeve gastroplasty: technical success and reproducibility in the bariatric population.
Endoscopy
PUBLISHED: 11-07-2014
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Background and aims: Novel endoscopic techniques have been developed as effective treatments for obesity. Recently, reduction of gastric volume via endoscopic placement of full-thickness sutures, termed endoscopic sleeve gastroplasty (ESG), has been described. Our aim was to evaluate the safety, technical feasibility, and clinical outcomes for ESG. Patient and methods: Between August 2013 and May 2014, ESG was performed on 10 patients using an endoscopic suturing device. Their weight loss, waist circumference, and clinical outcomes were assessed. Results: Mean patient age was 43.7 years and mean body mass index (BMI) was 45.2?kg/m(2). There were no significant adverse events noted. After 1 month, 3 months, and 6 months, excess weight loss of 18?%, 26?%, and 30?%, and mean weight loss of 11.5?kg, 19.4?kg, and 33.0?kg, respectively, were observed. The differences observed in mean BMI and waist circumference were 4.9?kg/m(2) (P?=?0.0004) and 21.7?cm (P?=?0.003), respectively. Conclusions: ESG is effective in achieving weight loss with minimal adverse events. This approach may provide a cost-effective outpatient procedure to add to the steadily growing armamentarium available for treatment of this significant epidemic.
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Evolving directions in obesity management.
J Fam Pract
PUBLISHED: 09-09-2014
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Over the past decade, treatment for obesity has been limited because of an incomplete understanding of the pathophysiology of obesity, lack of recognition of it as a disease, and limited efficacy of treatment options. Safety concerns related to medical and surgical approaches for obesity have also been a major barrier. The challenging nature of obesity management is reflected in a survey of primary care physicians which indicated that treating patients with obesity can be as difficult as treating patients with nicotine or alcohol dependence.
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Recombinant human leptin does not alter gut hormone levels after gastric bypass but may attenuate sweet cravings.
Int J Endocrinol
PUBLISHED: 02-19-2014
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Bariatric surgery improves glucose homeostasis and alters gut hormones partly independent of weight loss. Leptin plays a role in these processes; levels are decreased following bariatric surgery, creating a relative leptin insufficiency. We previously showed that leptin administration in a weight-reduced state after Roux-en-Y gastric bypass (RYGB) caused no further weight loss. Here, we discuss the impact of leptin administration on gut hormones, glucostasis, and appetite. Weight stable women after RYGB were randomized to receive placebo or recombinant human metreleptin (0.05?mg/kg twice daily). At weeks 0 and 16, a liquid meal challenge was performed. Glucose, insulin, C-peptide, GLP-1, PYY, glucagon, and ghrelin (total, acyl, and desacyl) were measured fasting and postprandially. Appetite was assessed using a visual analog scale. Mean post-op period was 53 ± 2.3 months; mean BMI was 34.6 ± 0.2?kg/m(2). At 16 weeks, there was no significant change in weight within or between groups. Fasting PYY was significantly different between groups and the leptin group had lower sweets craving at week 16 than the placebo group (P < 0.05). No other differences were observed. Leptin replacement does not alter gut hormones or glucostasis but may diminish sweet cravings compared to placebo in this population of post-RYGB women.
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Evaluation of phentermine and topiramate versus phentermine/topiramate extended-release in obese adults.
Obesity (Silver Spring)
PUBLISHED: 04-27-2013
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A 28-week, randomized, controlled trial compared the combination of phentermine and topiramate extended-release (PHEN/TPM ER) with its components as monotherapies and with placebo in obese adults.
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Obesity, adiposity, and dyslipidemia: a consensus statement from the National Lipid Association.
J Clin Lipidol
PUBLISHED: 03-18-2013
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The term "fat" may refer to lipids as well as the cells and tissue that store lipid (ie, adipocytes and adipose tissue). "Lipid" is derived from "lipos," which refers to animal fat or vegetable oil. Adiposity refers to body fat and is derived from "adipo," referring to fat. Adipocytes and adipose tissue store the greatest amount of body lipids, including triglycerides and free cholesterol. Adipocytes and adipose tissue are active from an endocrine and immune standpoint. Adipocyte hypertrophy and excessive adipose tissue accumulation can promote pathogenic adipocyte and adipose tissue effects (adiposopathy), resulting in abnormal levels of circulating lipids, with dyslipidemia being a major atherosclerotic coronary heart disease risk factor. It is therefore incumbent upon lipidologists to be among the most knowledgeable in the understanding of the relationship between excessive body fat and dyslipidemia. On September 16, 2012, the National Lipid Association held a Consensus Conference with the goal of better defining the effect of adiposity on lipoproteins, how the pathos of excessive body fat (adiposopathy) contributes to dyslipidemia, and how therapies such as appropriate nutrition, increased physical activity, weight-management drugs, and bariatric surgery might be expected to impact dyslipidemia. It is hoped that the information derived from these proceedings will promote a greater appreciation among clinicians of the impact of excess adiposity and its treatment on dyslipidemia and prompt more research on the effects of interventions for improving dyslipidemia and reducing cardiovascular disease risk in overweight and obese patients.
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A randomized, phase 3 trial of naltrexone SR/bupropion SR on weight and obesity-related risk factors (COR-II).
Obesity (Silver Spring)
PUBLISHED: 02-15-2013
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To examine the effects of naltrexone/bupropion (NB) combination therapy on weight and weight-related risk factors in overweight and obese participants.
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Randomized double-blind placebo-controlled study of leptin administration after gastric bypass.
Obesity (Silver Spring)
PUBLISHED: 02-10-2013
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Obese individuals have high levels of circulating leptin and are resistant to the weight-reducing effect of leptin administration at physiological doses. Although Roux-en-Y gastric bypass (RYGB) is an effective weight loss procedure, there is a plateau in weight loss and most individuals remain obese. This plateau may be partly due to the decline in leptin resulting in a state of relative leptin insufficiency. The main objective of this study was to determine whether leptin administration to post-RYGB patients would promote further weight reduction.
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Emerging pharmacotherapy for obesity.
Expert Opin Emerg Drugs
PUBLISHED: 08-12-2011
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Obesity is a rapidly increasing global health problem. The rates of obesity have tripled over the past three decades and are predicted to rise even further. The need for safe and effective therapies is great and has gone unmet.
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Implantable gastric stimulator does not prevent the increase in plasma ghrelin levels that occurs with weight loss.
Obesity (Silver Spring)
PUBLISHED: 06-16-2011
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The SHAPE (Screened Health Assessment and Pacer Evaluation) trial was a 24 month randomized multicenter placebo-controlled study to determine the efficacy of an implantable gastric stimulator (IGS) for weight loss. This report is an investigator-initiated sub-study at one site designed to assess whether IGS affects plasma levels of ghrelin and peptide YY (PYY). The device was implanted in all subjects but was activated in the Treatment group (n = 7, BMI = 41.5 ± 2.0 kg/m2) and remained inactive in the Control (n = 6, BMI = 39.5 ± 1.7 kg/m2) during the first 12 months. IGS was activated in both groups during months 12-24. Fasting venous blood was drawn at months 0, 12, and 24 and an oral glucose tolerance test (OGTT) was performed at month 12. Although there was no difference in weight loss at 6 months (Control: -6.6 ± 1.5% vs. Treatment: -6.2 ± 1.4%), at 24 months the Control group exhibited weight gain from baseline (+2.2 ± 1.5%) that was significantly different from the weight loss in the Treatment group (-1.9 ± 1.4%; P < 0.05). At 12 months, fasting ghrelin was significantly increased (P < 0.05) in the Treatment group (285 ± 35 to 336 ± 35 pg/ml; weight change, -4.9 ± 1.4%), but not in the Control (211 ± 36 to 208 ± 35 pg/ml; weight change, -3.4 ± 1.5%). No significant change was observed in postprandial suppression of plasma ghrelin or in fasting and postprandial PYY levels. In conclusion, IGS does not prevent the increase in fasting plasma ghrelin levels associated with weight loss. Further studies are needed to determine whether changes in technology can improve weight loss and maintenance, perhaps using gut hormones as biomarkers of possible efficacy.
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Efficacy and safety of CP-945,598, a selective cannabinoid CB1 receptor antagonist, on weight loss and maintenance.
Obesity (Silver Spring)
PUBLISHED: 02-03-2011
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Three double-blind, placebo-controlled, three-parallel-group, multicenter phase 3 trials were conducted to assess the efficacy and safety of CP-945,598 for weight loss and weight-loss maintenance. Two trials were designed to be 2 years in duration (in obese and overweight patients) and one as a 1-year study (in obese and overweight patients with type 2 diabetes). However, the 2-year trials and the CP-945,598 development program were terminated before completion due to changing regulatory perspectives of CB1 receptor-related drugs. In total, 1,253 and 2,536 participants in the two 2-year multinational and North American studies were randomized to 10-mg CP-945,598 (n = 360; 718); 20-mg CP-945,598 (n = 534, 1,084) and placebo (n = 359, 734), respectively; and 975 participants were randomized to 10-mg CP-945,598 (n = 318); 20-mg CP-945,598 (n = 320); and placebo (n = 337) in the 1-year multinational diabetes trial. Baseline demographics were similar between treatment groups within each trial. One year of treatment with CP-945,598 resulted in a dose-related mean percentage reduction from baseline body-weight in all trials. A significant proportion of all participants also achieved 5% and 10% weight loss after 1 year. In participants with mainly well-controlled type 2 diabetes, the combination of lifestyle and CP-945,598 induced substantial improvements in glycemic control. The most frequent adverse events (AEs) for CP-945,598 were: diarrhea, nausea, nasopharyngitis, and headache. Self-reported experiences of anxiety and suicidal thoughts were higher with CP-945,598 than placebo, as were the incidence of depression and depressed mood. However, the reported increases in psychiatric symptoms were not consistently dose dependent.
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Impact of waist circumference difference on health-care cost among overweight and obese subjects: the PROCEED cohort.
Value Health
PUBLISHED: 01-26-2010
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To estimate the incremental effect of waist circumference (WC) on health-care costs among overweight and obese subjects after adjusting for body mass index (BMI).
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Enhanced weight loss following coadministration of pramlintide with sibutramine or phentermine in a multicenter trial.
Obesity (Silver Spring)
PUBLISHED: 01-21-2010
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Preclinical evidence suggests that pharmacotherapy for obesity using combinations of agents targeted at distinct regulatory pathways may produce robust additive or synergistic effects on weight loss. This randomized placebo-controlled trial examined the safety and efficacy of the amylin analogue pramlintide alone or in combination with either phentermine or sibutramine. All patients also received lifestyle intervention. Following a 1-week placebo lead-in, 244 obese or overweight, nondiabetic subjects (88% female; 41 +/- 11 years; BMI 37.7 +/- 5.4 kg/m(2); weight 103 +/- 19 kg; mean +/- s.d.) received placebo subcutaneously (sc) t.i.d., pramlintide sc (120 microg t.i.d.), pramlintide sc (120 microg t.i.d.) + oral sibutramine (10 mg q.a.m.), or pramlintide sc (120 microg t.i.d.) + oral phentermine (37.5 mg q.a.m.) for 24 weeks. Treatment was single-blind for subjects receiving subcutaneous medication only and open-label for subjects in the combination arms. Weight loss achieved at week 24 with either combination treatment was greater than with pramlintide alone or placebo (P < 0.001; 11.1 +/- 1.1% with pramlintide + sibutramine, 11.3 +/- 0.9% with pramlintide + phentermine, -3.7 +/- 0.7% with pramlintide; -2.2 +/- 0.7% with placebo; mean +/- s.e.). Elevations from baseline in heart rate and diastolic blood pressure were demonstrated with both pramlintide + sibutramine (3.1 +/- 1.2 beats/min, P < 0.05; 2.7 +/- 0.9 mm Hg, P < 0.01) and pramlintide + phentermine (4.5 +/- 1.3 beats/min, P < 0.01; 3.5 +/- 1.2 mm Hg, P < 0.001) using 24-h ambulatory monitoring. However, the majority of subjects receiving these treatments remained within normal blood pressure ranges. These results support the potential of pramlintide-containing combination treatments for obesity.
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Ten putative contributors to the obesity epidemic.
Crit Rev Food Sci Nutr
PUBLISHED: 12-05-2009
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The obesity epidemic is a global issue and shows no signs of abating, while the cause of this epidemic remains unclear. Marketing practices of energy-dense foods and institutionally-driven declines in physical activity are the alleged perpetrators for the epidemic, despite a lack of solid evidence to demonstrate their causal role. While both may contribute to obesity, we call attention to their unquestioned dominance in program funding and public efforts to reduce obesity, and propose several alternative putative contributors that would benefit from equal consideration and attention. Evidence for microorganisms, epigenetics, increasing maternal age, greater fecundity among people with higher adiposity, assortative mating, sleep debt, endocrine disruptors, pharmaceutical iatrogenesis, reduction in variability of ambient temperatures, and intrauterine and intergenerational effects as contributing factors to the obesity epidemic are reviewed herein. While the evidence is strong for some contributors such as pharmaceutical-induced weight gain, it is still emerging for other reviewed factors. Considering the role of such putative etiological factors of obesity may lead to comprehensive, cause specific, and effective strategies for prevention and treatment of this global epidemic.
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Obesity as a disease state: a new paradigm for diagnosis and treatment.
Clin Cornerstone
PUBLISHED: 10-01-2009
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While global prevalence of obesity continues to increase dramatically, treatment options remain less than optimal. The etiology of obesity is multifactorial, ranging from lifestyle choices such as excess food intake and insufficient physical activity, to use of medications that have weight gain as an undesirable side effect. Economic and political determinants of available foodstuffs and even social networks may also contribute to obesity. Successful management of obesity requires the understanding and acceptance of a new paradigm that identifies obesity as a disease--one defined by waist circumference--that requires treatment. Obesity meets all accepted criteria of a medical disease, including a known etiology, recognized signs and symptoms, and a range of structural and functional changes that culminate in pathologic consequences. Excess adipose tissue acts as an endocrine organ to produce excess free fatty acids, as well as tumor necrosis factor-alpha, interleukin-6, leptin, and plasminogen activator inhibitor-1. These bioactive molecules are associated with hyperinsulinemia, hyperglycemia, insulin resistance, development of diabetes, endothelial damage, and the onset and progression of atherosclerotic lesions. Options for treating obesity include lifestyle modifications (dietary changes, increased physical activity, behavior modification) and, for the morbidly obese, surgery. Lifestyle modification is rarely successful over the long term; therefore, addition of pharmacotherapy should be considered for obese individuals who have difficulty achieving and maintaining weight goals with lifestyle modifications alone. Several weight loss drugs are available for long-term use, with others in various stages of clinical development.
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When prevention fails: obesity treatment strategies.
Am. J. Med.
PUBLISHED: 05-05-2009
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The obesity epidemic has resulted in increasingly urgent calls for large-scale prevention strategies. Meanwhile, effective treatment approaches that result in sustainable weight loss are needed to attenuate the cardiometabolic risks that may lead to comorbid illnesses and early mortality. Public education efforts geared toward those afflicted with obesity should emphasize that a relatively modest reduction in body weight dramatically reduces disease risk, thereby improving overall long-term health. Setting realistic weight loss goals with patients should reduce the overwhelming frustration often associated with the belief that large amounts of weight loss are needed for improved health. This misconception often impedes overweight and obese individuals from seeking treatment. Effective strategies are available to help overweight and obese individuals achieve reasonable weight loss goals. Important challenges exist in preventing weight regain following weight loss intervention. Studies are underway to identify new therapeutic strategies to effectively reduce weight, as well as to provide long-term data on successful weight loss maintenance strategies.
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Obesity-related hypertension: pathogenesis, cardiovascular risk, and treatment--a position paper of the The Obesity Society and The American Society of Hypertension.
Obesity (Silver Spring)
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In light of the worldwide epidemic of obesity, and in recognition of hypertension as a major factor in the cardiovascular morbidity and mortality associated with obesity, The Obesity Society and The American Society of Hypertension agreed to jointly sponsor a position paper on obesity-related hypertension to be published jointly in the journals of each society. The purpose is to inform the members of both societies, as well as practicing clinicians, with a timely review of the association between obesity and high blood pressure, the risk that this association entails, and the options for rational, evidenced-based treatment. The position paper is divided into six sections plus a summary as follows: pathophysiology, epidemiology and cardiovascular risk, the metabolic syndrome, lifestyle management in prevention and treatment, pharmacologic treatment of hypertension in the obese, and the medical and surgical treatment of obesity in obese hypertensive patients.
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Obesity-related hypertension: pathogenesis, cardiovascular risk, and treatment: a position paper of The Obesity Society and the American Society of Hypertension.
J Clin Hypertens (Greenwich)
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In light of the worldwide epidemic of obesity, and in recognition of hypertension as a major factor in the cardiovascular morbidity and mortality associated with obesity, The Obesity Society and the American Society of Hypertension agreed to jointly sponsor a position paper on obesity-related hypertension to be published jointly in the journals of each society. The purpose is to inform the members of both societies, as well as practicing clinicians, with a timely review of the association between obesity and high blood pressure, the risk that this association entails, and the options for rational, evidenced-based treatment. The position paper is divided into six sections plus a summary as follows: pathophysiology, epidemiology and cardiovascular risk, the metabolic syndrome, lifestyle management in prevention and treatment, pharmacologic treatment of hypertension in the obese, and the medical and surgical treatment of obesity in obese hypertensive patients.
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Causes of obesity.
Abdom Imaging
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The prevalence of obesity has been rising steadily over the last several decades and is currently at unprecedented levels: more than 68% of US adults are considered overweight, and 35% are obese (Flegal et al., JAMA 303:235-241, 2010). This increase has occurred across every age, sex, race, and smoking status, and data indicate that segments of individuals in the highest weight categories (i.e., BMI > 40 kg/m(2)) have increased proportionately more than those in lower BMI categories (BMI < 35 kg/m(2)). The dramatic rise in obesity has also occurred in many other countries, and the causes of this increase are not fully understood (Hill and Melanson, Med Sci Sports Exerc 31:S515-S521, 1999).
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

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.