Download or read book Mechanisms of Conjugated Linoleic Acid on Insulin Resistance Hepatic Steatosis and Adiposity written by Angela Ann Wendel and published by . This book was released on 2007 with total page 216 pages. Available in PDF, EPUB and Kindle. Book excerpt: The significant depletion of adipose in mice by CLA may contribute to the lipodystrophic-like effects that accompany. The final objective of this research was to determine mechanisms by which CLA reduces adipose mass. Six-week old, male ob/ob mice were fed either a control diet (CON) or a diet supplemented with 1.5% mixed isomer CLA (CLA) for 4 weeks. A third group of mice (LEPTIN) were fed the control diet and received daily, intraperitoneal injections of 1 mg/kg BW recombinant leptin as a positive control for adipose depletion in ob/ob mice. The depletion of adipose tissue by CLA was accompanied by the acquirement of brown adipose-like characteristics, such as increased CPT-1b, PGC-1alpha, and UCP-1, in the white adipose of CLA-fed mice. This alteration may facilitate the reduction of adipose mass by increasing mitochondrial oxidation and energy dissipation. However, it appears that CLA does not increase UCP-1 through beta3AR signaling.

Download or read book Prevention of CLA induced Insulin Resistance and Nonalcoholic Fatty Liver Disease by Docosahexaenoic Acid in Mice written by Dawn Fedor and published by . This book was released on 2013 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Insulin resistance (IR) is a condition in which normal amounts of insulin fail to maintain normal blood glucose because of decreased responsiveness of muscle (glucose uptake), liver (inhibition of gluconeogenesis) and adipocytes (inhibition of lipolysis). IR is often associated with nonalcoholic fatty liver disease (NAFLD), the most common liver disease in adults and children in the Western world. Results from human epidemiological studies indicate that n-3 PUFA reduce the development of IR and NAFLD although the mechanisms involved are poorly understood. Our lab previously showed that concomitant supplementation of 1.5% docosahexaenoic acid (22:6 n-3; DHA) with 0.5% t10, c12- conjugated linoleic acid (18:2 n-6; CLA) prevented the CLA-induced NAFLD and IR. The effective dose of DHA, the mechanisms involved and the effect of CLA on fatty acid compositions of adipose tissue and muscle, and whether DHA can prevent those CLA-induced changes in fatty acid composition is not known. In the first study, we examined the ability of DHA (0.5 and 1.5%) to prevent increases in NAFLD and homeostatic model assessment of insulin resistance (HOMA-IR) induced by CLA (0.5%) when fed concomitantly for 4 weeks to C57BL/6N female mice. We also examined changes in expression of hepatic genes involved in fatty acid synthesis and oxidation. CLA supplementation increased liver triglycerides (TG) and HOMA-IR by 221 and 547%, respectively, and decreased mass of adipose depots by 65-90%. When fed concomitantly, 0.5% and 1.5% DHA prevented CLA-induced increases in liver TG and circulating insulin with varying efficiency, but neither dose of DHA prevented the loss in adipose tissue mass. In CLA + DHA 0.5 % group the liver TG did not differ from those in the control group, but circulating insulin and HOMA-IR were 285 and 264 %, respectively, greater than those in the control group. In the CLA + DHA 1.5% group liver TG were 54% lower than those in the control group, but circulating insulin concentration and HOMA-IR did not differ between these two groups. CLA increased the expression of hepatic genes involved in fatty acid synthesis and decreased the expression of genes involved in fatty acid oxidation. 1.5% DHA prevented changes in the expression of hepatic genes caused by CLA, which may be a possible mechanism contributing to the prevention of TG accumulating in the liver. Based on these results, we further studied the 1.5% DHA diet. We investigated the effects of 1.5% DHA concomitantly fed with CLA on fatty acid compositions of liver, adipose, and muscle lipids in the same mice, as well as expression of genes involved in adipose fatty acid metabolism. CLA supplementation decreased total hepatic n-3 PUFA concentration. DHA not only prevented the CLA-induced changes in liver fat, but also increased n-3 PUFA by >350% as compared with the control group. CLA decreased adipose weight and the expression of genes involved in fatty acid synthesis, oxidation, and uptake, and increased that of UCP2 in the adipose. Supplementing DHA along with CLA increased adipose n-3 PUFA by >1000% compared with control group, but did not prevent the CLA-induced changes in mass or gene expression. Both CLA and DHA were incorporated into muscle lipids, but had minor effects on FA composition. In conclusion, liver, adipose tissue, and muscle responded differently to CLA and DHA supplementation. CLA was more potent than DHA in altering depot fat and insulin concentration. DHA prevented CLA-induced increase in liver fat but not loss of adipose mass. CLA and DHA were preferentially incorporated into adipose tissue lipids, but they had only modest effects on the overall fatty acid composition of the adipose tissue. The largest changes in fatty acid composition were seen in the liver and smallest in muscle lipids.

Download or read book Anti obesity Mechanisms of Conjugated Linoleic Acid CLA written by Wan Shen and published by . This book was released on 2015 with total page 176 pages. Available in PDF, EPUB and Kindle. Book excerpt: "Overweight and obesity are the most widespread nutritional diseases in the U.S., which greatly increase chronic disease risks and mortality. Therefore, it is urgent to develop a relatively efficacious and safe strategy for the weight management. Consumption of conjugated linoleic acid (CLA) supplements or one of its isomers, trans-10, cis-12 (10,12) CLA, has consistently demonstrated reductions in body weight or body fat in human and animal studies. Our lab has demonstrated that 10,12 CLA triggered calcium release from endoplasmic reticulum in human primary adipocytes, which activated downstream inflammatory signaling, resulting in impaired uptake of glucose and fatty acid, and delipidation. However, the upstream signals responsible for these actions are unknown. Therefore, my Aim 1 investigated the upstream mechanism by which 10,12 CLA increases intracellular calcium and inflammatory signaling in human primary adipocytes. The results indicated that phospholipase C plays an important role in 10,12 CLA-mediated activation of intracellular calcium accumulation, inflammatory signaling, delipidation, and insulin resistance in human primary adipocytes. It has been demonstrated that 10,12 CLA increased mRNA levels and protein levels of cyclooxygenase-2 (COX-2) and pro-inflammatory prostaglandins, which have been linked to increased energy expenditure associated with white adipose tissue (WAT) browning and uncoupling of ATP synthesis. It also has been shown that relatively high doses of 10,12 CLA lead to more significant reductions in body fat, but cause a greater level of inflammation, insulin resistance, and steatosis in animals. Therefore, Aims 2 and Aim 3 determined the extent to which a relative low dose of 10,12 CLA or a CLA isomer mixture increases markers of browning in mice and its dependence in inflammatory signaling. In Aim 2, a low threshold dose of 10,12 CLA was found that prevented body fat accumulation with minimum metabolic side-effects in non-obese mice. It was also found that 10,12 CLA-induced browning in WAT was accompanied by increases in mRNA levels of COX-2 and other markers of inflammation. In Aim 3, a relatively low dose of 10,12 CLA reduced body fat and increased browning of WAT in overweight mice, which were independent of inflammatory signaling. Collectively, these findings provide critical insights for the development of reliable dietary strategies for people who take CLA as method to lose weight. However, we still do not know (i) if 10,12 CLA supplementation would effectively reduce body fat in overweight mice when they are continuously fed an American-type, high-fat diet; (ii) potential risks of impaired regulation of body temperature, inflammation, and steatosis due to 10,12 CLA consumption in high fat-fed mice; and (iii) potential mechanisms by which 10,12 CLA reduces body fat in high fat-fed mice."--Abstract from author supplied metadata.

Download or read book Conjugated Linoleic Acid CLA in Liver and Adipose Metabolism written by Amy Dianne Noto and published by . This book was released on 2005 with total page 294 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Anti adipogenic Mechanism of Conjugated Linoleic Acid written by Kihwa Kang and published by . This book was released on 2003 with total page 176 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Mechanisms by which Conjugated Linoleic Acid Causes Human Adipocyte Delipidation written by Soonkyu Chung and published by . This book was released on 2006 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: "Obesity is an important health issue, having risen to epidemic proportions in the U.S. Use of conjugated linoleic acid (CLA), positional and geometric isomers of linoleic acid, has received recent attention due to its potential health benefits including the reduction of fat mass in animals. However, the effectiveness and safety of CLA consumption in humans remains unclear. Our group previously reported that trans-10, cis-12 CLA impaired the conversion of preadipocytes into lipid-filled adipocytes (e.g., differentiation) and caused adipocyte delipidation that involved inflammatory cytokines in a human cell model. However, the isomer-specific mechanism for these events was unknown. Thus, this research examined mechanisms by which trans-10, cis-12 CLA induced adipocyte delipidation, inflammation, and insulin resistance in primary cultures of human adipocytes. Delipidation of adipocytes by trans-10, cis-12 CLA was accompanied by increased lipolysis and changes in the morphology of lipid droplets and the expression and localization of proteins regulating lipid droplet metabolism. This process involved the translational control of adipose differentiated related protein (ADRP) through activation of mTOR/p70S6K/S6 signaling and transcriptional control of perilipin A. Prior to these morphological changes, it was shown that trans-10, cis-12 CLA promoted nuclear factor κB (NFκB) and mitogen activated protein kinase (MAPK) activation and subsequent induction of interleukin (IL)-6 which were, at least in part, responsible for trans-10, cis-12 CLA-mediated suppression of peroxisome proliferator activated receptor gamma (PPAR)γ target gene expression and insulin sensitivity in human adipocytes. The essential role of NFκB on CLA-induced inflammation was confirmed by using RNA interference. Further studies were conducted examining the localization and characterization of the inflammatory response, including the type of cells involved, using lipopolysaccharide (LPS) as the inflammatory agent. It was demonstrated that LPS-induced, NFκB-dependent proinflammatory cytokine expression was predominantly from preadipocytes, which led to, at least in part, the suppression of PPAR activity and adipogenic gene expression and insulin sensitivity. Collectively, these data support the emerging concept that adipose tissue is a dynamic endocrine organ with the capacity to generate inflammatory signals that impact glucose and lipid metabolism. Furthermore, human preadipocytes have the capacity to generate these inflammatory signals induced by trans-10, cis-12 CLA and LPS, subsequently causing insulin resistance in neighboring adipocytes. These studies also revealed that NFκB- and MAPK-signaling mediate inflammation and insulin resistance induced by CLA and LPS. Thus, although the trans-10, cis-12 isomer of CLA may decrease the size and lipid content of human adipocytes, it may also cause insulin resistance, which is a hallmark of type 2 diabetes."--Abstract from author supplied metadata.

Download or read book Differential Metabolic Effects in White and Brown Adipose Tissue by Conjugated Linoleic Acid Elicit Lipodystrophy associated Hepatic Insulin Resistance written by Michael B. Stout and published by . This book was released on 2011 with total page 138 pages. Available in PDF, EPUB and Kindle. Book excerpt: Abstract: The prevalence of obesity has risen substantially throughout the world in recent decades. Nonsurgical treatments for reducing adiposity remain paramount to diminishing obesity and its associated comorbidities. Conjugated linoleic acid has received considerable attention due to its ability to reduce body weight and adiposity in a number of species. The mechanisms responsible for adipose depletion by conjugated linoleic acid remain controversial and are not completely understood. The first objective of this research was to determine if conjugated linoleic acid altered adipose phenotype by inducing adaptive thermogenesis and increasing oxidative capacity. In this study, conjugated linoleic acid dramatically reduced weight gain and adipose mass. Additionally, conjugated linoleic acid induced the expression of numerous genes involved in adaptive thermogenesis in epididymal white adipose tissue. Lipid droplet morphology was unchanged by conjugated linoleic acid treatment, although mitochondrial density was increased in epididymal white adipose tissue. Unexpectedly, whole body oxygen consumption and body temperatures were reduced and unchanged by conjugated linoleic acid treatment, respectively. We attributed these observations to a significant reduction in brown adipose tissue with a concomitant compensatory response in epididymal white adipose tissue. Our data suggest that significant reductions in brown adipose tissue by conjugated linoleic acid initiates white adipose adaptive thermogenesis as a means to maintain body temperature.

Download or read book Role of Bioactive Compounds in the Regulation of Insulin Sensitivity written by Aparna Purushotham and published by . This book was released on 2007 with total page 197 pages. Available in PDF, EPUB and Kindle. Book excerpt: The effects of CLA were observed in the absence of decreases in adiposity, adipokines, body weight and food intake in Wistar rats suggesting that CLA is protective against hepatic TG accumulation in high fat-fed rats by modulating hepatic lipid metabolism.

Download or read book Regulation of Adiposity by Dietary Conjugated Linoleic Acid written by Xiaofang Xu and published by . This book was released on 2002 with total page 184 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Effect of Omega 3 Fatty Acids on T10 C12 conjugated Linoleic Acid Induced Insulin Resistance Non Alcoholic Fatty Liver Disease and Tissue Fatty Acid Composition written by Madhuri Vemuri and published by . This book was released on 2009 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Conjugated linoleic acid (CLA) refers to all the positional and geometric isomers of linoleic acid. The two most studied isomers are cis9, trans11-CLA and trans10, cis12-CLA. CLA supplements, often a mixture of the two isomers, have been popularly used for weight loss and other claimed health benefits. However supplementing CLA isomers, especially trans10, cis12-CLA has been shown to cause non alcoholic fatty liver disease (NAFLD) and insulin resistance (IR) in several animal models. Here we have confirmed that supplementing 0.5% trans10, cis12-CLA to C57BL/6 mice for 8 weeks causes NAFLD and IR. When CLA diets were concomitantly supplemented with omega-3 fatty acids docosahexaenoic acid (DHA) or eicosapentaenoic acid (EPA) at 1.5% (w/w) for 8 weeks, DHA prevented CLA induced IR, while EPA was ineffective. Both EPA and DHA prevented CLA induced fatty liver. CLA also reduced the plasma leptin and adiponectin concentrations, and both EPA and DHA partially restored plasma leptin, but only DHA partially restored the plasma adiponectin. In another experiment, concomitant supplementation of CLA diets with 0.5% of flaxseed oil (rich in alpha linolenic acid) also prevented IR and decreased liver weights and lipids compared with those in CLA group. CLA supplementation also altered lipid profile in liver, decreasing n-6 and n-3 wt% and increasing n-6:n-3 ratio. Concomitant supplementation with flaxseed oil increased n-6 and n-3 polyunsaturated (PUFA) in liver lipids and decreased the n-6:n-3 ratio compared to that in CLA group. Supplementing 0.5% (w/w) of purified c9, t11- or trans10, cis12-CLA to mice for 8 weeks altered fatty acid profile of tissues differently. c9, t11-CLA diet reduced MUFA wt% in liver, adipose tissue, and spleen, and reduced the spleen n-3 PUFAs significantly while increasing the n-6 PUFA wt% in all tissues except heart. In contrast, trans10, cis12-CLA reduced both the n-6 and n-3 PUFA wt% in liver and heart however increased the wt% of n-3 PUFAs in spleen. Considering the adverse health effects of trans10, cis12-CLA and of mixtures of CLA isomers on NAFLD, IR and tissue fatty acids, human use of CLA supplements should not be recommended.

Download or read book Nutrition in the Prevention and Treatment of Abdominal Obesity written by Ronald Ross Watson and published by Elsevier. This book was released on 2014-02-26 with total page 559 pages. Available in PDF, EPUB and Kindle. Book excerpt: Nutrition in the Prevention and Treatment of Abdominal Obesity focuses on the important roles that exercise, dietary changes, and foods play in promoting as well as reducing visceral fat. Nutritionists, dieticians, and healthcare providers seeking to address the abdominal obesity epidemic will use this comprehensive resource as a tool in their long-term goal of preventing chronic diseases, especially heart, vascular, and diabetic diseases. Experts from a broad range of disciplines are involved in dealing with the consequences of excessive abdominal fat: cardiology, diabetes research, studies of lipids, endocrinology and metabolism, nutrition, obesity, and exercise physiology. They have contributed chapters that define a range of dietary approaches to reducing risk and associated chronic diseases. They begin by defining visceral obesity and its major outcomes; they also discuss the importance and the challenges of dietary approaches to reduce abdominal obesity, as compared to clinical approaches, with major costs and risks. Offers detailed, well-documented reviews outlining the various dietary approaches to visceral obesity with their benefits and failures Includes chapters on types of foods, exercise, and supplements in reducing obesity and its chronic clinical companions, especially diabetes and cardiovascular disease Helps nutritionists, dieticians, and healthcare providers approach patients in making decision about nutritional therapies and clinical treatments for abdominal obesity, from an evidence-based perspective

Download or read book Diabetes Mellitus written by Derek LeRoith and published by Lippincott Williams & Wilkins. This book was released on 2004 with total page 1606 pages. Available in PDF, EPUB and Kindle. Book excerpt: Thoroughly revised and updated, this Third Edition encompasses the most recent advances in molecular and cellular research and describes the newest therapeutic modalities for type 1 and type 2 diabetes mellitus. Chapters by leading experts integrate the latest basic science and clinical research on diabetes mellitus and its complications. The text is divided into ten major sections, including extensive sections on therapeutics, diabetes during pregnancy, and complications. New chapters cover stem cell therapy for type 1 diabetes; genetics and treatment of obesity; new therapies to promote insulin action; vasculopathy; islet cell protocols; triglycerides in muscle; hypoglycemia in the adult; and the Diabetes Prevention Program.

Download or read book Nutrient Metabolism written by Martin Kohlmeier and published by Academic Press. This book was released on 2015-05-12 with total page 899 pages. Available in PDF, EPUB and Kindle. Book excerpt: Nutrient Metabolism, Second Edition, provides a comprehensive overview of the supply and use of nutrients in the human body and how the body regulates intake. Chapters detail the principles determining digestion and absorption of food ingredients and how these compounds and their metabolites get into the brain, cross the placenta and pass through the kidneys. Each nutrient’s coverage contains a nutritional summary that describes its function, its food sources, dietary requirements, potential health risks if deficient, and impact of excessive intake. This handbook contains the latest information on the scope of structures, processes, genes and cofactors involved in maintaining a healthy balance of nutrient supplies. Of interest to a wide range of professionals because nutrient issues connect to so many audiences, the book contains a useful link to dietary supplements. Latest research findings on health and clinical effects of nutrients and of interventions affecting nutrient supply or metabolism Each nutrient covered contains a nutritional summary describing its function, food sources, dietary requirements, potential health risks if deficient, and impact of excessive intake. Nutrient information immediately accessible--from source to effect--in one volume

Download or read book The Adipose Organ written by Saverio Cinti and published by . This book was released on 1999 with total page 94 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Advances in Conjugated Linoleic Acid Research written by Jean-Louis Sebedio and published by CRC Press. This book was released on 2020-03-05 with total page 338 pages. Available in PDF, EPUB and Kindle. Book excerpt: Advances in Conjugated Linoleic Acid Research, Volume 2 is the second book in a series devoted entirely to conjugated linoleic acid. This book has updated information on the analysis, biochemistry and applications of conjugated fatty acids in an attempt to make Volume 2, in conjunction with Volume 1 (published in 1999), the most comprehensive, up-to-date sources of CLA-related information available today. Both scientific and commercial views are presented, with the same data sometimes interpreted differently.

Download or read book Nutritional Pathophysiology of Obesity and its Comorbidities written by Susan Ettinger and published by Academic Press. This book was released on 2016-09-01 with total page 335 pages. Available in PDF, EPUB and Kindle. Book excerpt: Nutritional Pathophysiology of Obesity and Its Comorbidities: A Case-Study Approach challenges students and practitioners to understand the role of nutrients within the pathophysiology and development of disease, specifically those diseases which develop as a result of obesity. Through a case-based approach, the author presents complex clinical scenarios that require multiple treatment strategies, including targeted diet modification as an adjuvant to medical therapy. The book is divided into 9 modules and 5 appendices each of which covers aspects of obesity and its comorbidities. Within each module, a case is detailed with relevant history, laboratory and physical data, and follow-up information. Each case is followed by a resource section which delineates current understanding of the pathophysiology of the condition, as well as the actions of nutrients and food components shown to modify these processes. A "further readings" section cites current supporting clinical and basic literature as well as published guidelines. Explores how obesity is a key player in the pathophysiology of many diseases, including diabetes mellitus, chronic renal failure, hypertension, and atherosclerosis Integrates current understandings of the molecular mechanisms of nutrient action on the processes of disease development and treatment Presents students and early practitioners with complex clinical scenarios through a practical case-based approach

Download or read book Nonalcoholic Fatty Liver Disease An Issue of Clinics in Liver Disease E Book written by Arun J. Sanyal and published by Elsevier Health Sciences. This book was released on 2012-08-12 with total page 240 pages. Available in PDF, EPUB and Kindle. Book excerpt: Dr. Sanyal's expertise as Chairman of the Division of Hepatology at Virginia Commonwealth University and the breadth of his published articles in hepatology make him the perfect person to compile state-of-the-art reviews on the topic of NASH/fatty liver. The articles in this issue address the following topics: The Genetic Epidemiology of Nonalcoholic Fatty Liver Disease; Relevance of Liver Histology to Predict Clinically Meaningful Outcomes in NASH; Mechanisms of Simple Hepatic Steatosis; Cellular and Molecular Basis for Phenotype of Steatohepatitis; Mechanisms of Disease Progression in NASH: New Paradigms; Can NASH Be Diagnosed, Graded and Staged Non-Invasively?; Is NAFLD in Children the Same Disease as in Adults?; The Cardiovascular Link to NAFLD: A Critical Analysis; Impact of Behavioral Disturbances and Their Treatment on Obesity and NAFLD; and Management of NASH.