Swimming Improves High-fat Induced Insulin Resistance By Regulating Lipid And Energy Metabolism And The Insulin Pathway In Rats
Swimming improves high-fat induced insulin resistance by regulating lipid and energy metabolism and the insulin pathway in rats Affiliations: Department of Endocrinology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong 250021, P.R. China, Department of Endocrinology, General Hospital of Hebei, Shijiazhuang, Hebei 050051, P.R. China Published online on: April 9, 2014 Metrics: HTML 0 views | PDF 0 views Cited By (CrossRef): 0 citations In this study, we aimed to determine the preventive and therapeutic effects of swimming on insulin resistance in high-fat-fed rats. Sprague-Dawley rats were divided into 4groups and fed for 8 weeks as follows: i) the control (Con) group fed a control diet; ii) the high-fat (HF) group fed a high-fat diet; iii) the treatment (ST) group fed a high-fat diet and trained with swimming from the 4th week; and iv) the prevention (SP) group fed a high-fat diet and trained with swimming from the 1stweek of the experiment. A hyperinsulinemiceuglycemic clamp was used to evaluate the insulin sensitivity of the rats. The ultrastructure of the liver cells was observed by electron microscopy. Hepatic lipid accumulation was observed by OilRedO staining. Quantitative RT-PCR and western blot analysis were performed to detect the expression of proteins related to lipid metabolism, energy metabolism and insulin signaling transduction. After 8weeks of feeding, compared with the Con group, the glucose infusion rate (GIR) was significantly decreased; a significant lipid accumulation was observed in the liver, while the ultrastructure of the liver cells was damaged in the HF group. Proteins related to lipid metabolism in the liver and skeletal muscle, including FAT and FABP were upregulated, while CPT1 and PPAR levels were downregulated in the HF Continue reading >>
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Review Article Exercise And Obesity-induced Insulin Resistance In Skeletal Muscle
ABSTRACT The skeletal muscle in our body is a major site for bioenergetics and metabolism during exercise. Carbohydrates and fats are the primary nutrients that provide the necessary energy required to maintain cellular activities during exercise. The metabolic responses to exercise in glucose and lipid regulation depend on the intensity and duration of exercise. Because of the increasing prevalence of obesity, recent studies have focused on the cellular and molecular mechanisms of obesity-induced insulin resistance in skeletal muscle. Accumulation of intramyocellular lipid may lead to insulin resistance in skeletal muscle. In addition, lipid intermediates (e.g., fatty acyl-coenzyme A, diacylglycerol, and ceramide) impair insulin signaling in skeletal muscle. Recently, emerging evidence linking obesity-induced insulin resistance to excessive lipid oxidation, mitochondrial overload, and mitochondrial oxidative stress have been provided with mitochondrial function. This review will provide a brief comprehensive summary on exercise and skeletal muscle metabolism, and discuss the potential mechanisms of obesity-induced insulin resistance in skeletal muscle. Continue reading >>
Prevention Of Fat-induced Insulin Resistance By Salicylate.
Prevention of fat-induced insulin resistance by salicylate. Howard Hughes Medical Institute, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06536-8012, USA. Insulin resistance is a major factor in the pathogenesis of type 2 diabetes and may involve fat-induced activation of a serine kinase cascade involving IKK-beta. To test this hypothesis, we first examined insulin action and signaling in awake rats during hyperinsulinemic-euglycemic clamps after a lipid infusion with or without pretreatment with salicylate, a known inhibitor of IKK-beta. Whole-body glucose uptake and metabolism were estimated using [3-(3)H]glucose infusion, and glucose uptake in individual tissues was estimated using [1-(14)C]2-deoxyglucose injection during the clamp. Here we show that lipid infusion decreased insulin-stimulated glucose uptake and activation of IRS-1-associated PI 3-kinase in skeletal muscle but that salicylate pretreatment prevented these lipid-induced effects. To examine the mechanism of salicylate action, we studied the effects of lipid infusion on insulin action and signaling during the clamp in awake mice lacking IKK-beta. Unlike the response in wild-type mice, IKK-beta knockout mice did not exhibit altered skeletal muscle insulin signaling and action following lipid infusion. In summary, high-dose salicylate and inactivation of IKK-beta prevent fat-induced insulin resistance in skeletal muscle by blocking fat-induced defects in insulin signaling and action and represent a potentially novel class of therapeutic agents for type 2 diabetes. Turning down insulin signaling. [J Clin Invest. 2001] Images from this publication. See all images (7) Free text Metabolic parameters and insulin-stimulated whole-body and skeletal muscle (soleus) g Continue reading >>
P24sucrose- And High Fat-induced Insulin Resistance Leads To Endothelial Dysfunction And Is Associated With Ketohexokinase Activation | Heart
P24 Sucrose- and high fat-induced insulin resistance leads to endothelial dysfunction and is associated with ketohexokinase activation P24 Sucrose- and high fat-induced insulin resistance leads to endothelial dysfunction and is associated with ketohexokinase activation 1Division of Cardiovascular and Diabetes Research, Leeds Institute for Cardiovascular and Metabolic Medicine, LIGHT Laboratories, University of Leeds, Clarendon Way, Leeds, UK 2Leeds Institute of Biomedical and Clinical Sciences, Wellcome Trust Brenner Building (level 9), St Jamess University Hospital, Beckett Street, Leeds, UK Introduction Cardiovascular diseases affect an increasing number of people and are one of the major causes of mortality. Over-consumption of fructose, widely used in soft drinks, compromises normal insulin transduction pathways, leading to impaired insulin signalling. Fructose is mainly metabolised by the enzyme ketohexokinase (KHK) in the liver. However, the mechanism underlying fructose-induced insulin resistance and endothelial dysfunction remains unknown. We aimed to investigate the role of KHK in mediating these effects. Methods C57/BL6 mice were fed with three different diets for 20 weeks, namely low-fat (LFD), high-fat (HFD) and high-fat supplemented with sucrose (HFHS). Glucose and insulin tolerance tests were carried out after 5th, 11th and 16th weeks. Levels of various proteins were assessed by Western blotting. Endothelial function was analysed by measuring isometric tensions in organ bath set-ups. Results Glucose clearance and insulin sensitivity were decreased after 5, 11 and 16 weeks of HFHS diet. Moreover, fasting glucose and plasma insulin levels of HFHS mice were increased compared to LFD and HFD. IR-beta expression and IRS-1 levels were decreased in HFD and HFHS. Continue reading >>
High-fat Diet-induced Insulin Resistance In Single Skeletal Muscle Fibers Is Fiber Type Selective
Skeletal muscle is the major site for insulin-stimulated glucose disposal, and muscle insulin resistance confers many negative health outcomes. Muscle is composed of multiple fiber types, and conventional analysis of whole muscles cannot elucidate fiber type differences at the cellular level. Previous research demonstrated that a brief (two weeks) high fat diet (HFD) caused insulin resistance in rat skeletal muscle. The primary aim of this study was to determine in rat skeletal muscle the influence of a brief (two weeks) HFD on glucose uptake (GU) ± insulin in single fibers that were also characterized for fiber type. Epitrochlearis muscles were incubated with [3H]-2-deoxyglucose (2DG) ± 100 µU/ml insulin. Fiber type (myosin heavy chain expression) and 2DG accumulation were measured in whole muscles and single fibers. Although fiber type composition of whole muscles did not differ between diet groups, GU of insulin-stimulated whole muscles from LFD rats significantly exceeded HFD values (P < 0.005). For HFD versus LFD rats, GU of insulin-stimulated single fibers was significantly (P < 0.05) lower for IIA, IIAX, IIBX, IIB, and approached significance for IIX (P = 0.100), but not type I (P = 0.776) fibers. These results revealed HFD-induced insulin resistance was attributable to fiber type selective insulin resistance and independent of altered fiber type composition. Skeletal muscle is the major site for insulin-stimulated glucose disposal1, and skeletal muscle insulin resistance is a primary and essential event in the progression to type 2 diabetes2. Even in the absence of type 2 diabetes, insulin resistance confers negative health outcomes3. It is important to understand the processes responsible for insulin resistance of the skeletal muscle to develop interventions Continue reading >>
Consumption Of A Mango Fruit Powder Protects Mice From High-fat Induced Insulin Resistance And Hepatic Fat Accumulation
Abstract Background/Aims: The aim of this study was to gain more insight into the beneficial effects of mango fruit powder on the early metabolic adverse effects of a high-fat diet. Methods: The progressive dose-response effects of mango fruit powder on body composition, circulating parameters, and the expression of genes related to fatty acid oxidation and insulin sensitivity in key tissues were studied in mice fed a moderate (45%) high-fat diet. Results: Findings suggest that mango fruit powder exerts physiological protective effects in the initial steps of insulin resistance and hepatic lipid accumulation induced by a high-fat diet in mice. Moreover, AMPK and SIRT1 appear as key regulators of the observed improvement in fatty acid oxidation capacity, as well as of the improved insulin sensitivity and the increased glucose uptake and metabolism through the glycolytic pathway capacity in liver and skeletal muscle. Conclusion: In summary, this study provides evidence that the functional food ingredient (CarelessTM) from mango fruit prevents early metabolic alterations caused by a high-fat diet in the initial stages of the metabolic syndrome. © 2017 The Author(s). Published by S. Karger AG, Basel Introduction Dysregulated glucose and lipid metabolism and, thus, energy homeostasis are early events in the development of insulin resistance, which in turn may lead to obesity and diabetes mellitus type 2. The overall prevalence of insulin resistance in developed societies is high, with 11.5-14.0% of the European population [1], 20% of adults in Japan [2], and nearly 30% of adult Americans [3] being afflicted. The insensitivity of peripheral tissues to the effects of insulin starts when the nutrient storage metabolic pathways are exposed to persistent energy excess, surpassin Continue reading >>
Fat Induced Insulin Resistance And Atherosclerosis Boden, Guenther Temple University, Philadelphia, Pa, United States
Fat Induced Insulin Resistance and Atherosclerosis Obesity and several other risk factors for atherosclerotic vascular disease (ASVD) including hypertension, dyslipidemia and type 2 diabetes are associated with insulin resistance (IR). It has been suspected, therefore, that IR is an important factor in the pathogenesis of ASVD although the nature of the connection between IR and ASVD has remained elusive. Free fatty acids (FFAs) have been established as a major link between obesity and IR based on evidence showing that most obese people have elevated plasma FFAs and that acute as well as chronic elevation of plasma FFAs cause IR. Recent data have shown that FFA induced IR was accompanied by intramyocellular (IMCL) accumulation of fat and diacylglycerol (DAG, a by-product of IMCL FFA reesterification to fat) by activation of protein kinase C (PKC) Beta II and delta (serine kinases known to be activated by DAG and to cause IR in rodents) and by a drastic (70%) reduction of IMCL IkappaB-alpha, (the inhibitor of the NFkappaB pathway which is known to be strongly pro-inflammatory and atherogenic). We propose to strengthen this putative link between FFA induced IR and ASVD by testing the following hypotheses: 1) that FFA induced activation of the serine kinases PKC beta II and delta and perhaps IkappaB kinase (IKK) in human muscle is associated with a decrease in insulin stimulated tyrosine phosphorylation of IRS-1 and of IRS-1 associated PI3 kinase; 2) that these changes precede the development of IR; 3) that the decrease in IkappaB-alpha results in activation of NFkappaB; 4) that PKC and IKK are involved in producing IR and activation of the IkappaB/NFkappaB pathway and 5) that the same mechanisms operative in healthy volunteers are also operative in patients with T2DM. We Continue reading >>
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Unaltered Prion Pathogenesis In A Mouse Model Of High-fat Diet-induced Insulin Resistance
Unaltered Prion Pathogenesis in a Mouse Model of High-Fat Diet-Induced Insulin Resistance Affiliation Institute of Neuropathology, University Hospital Zurich, Zurich, Switzerland Affiliation Institute of Neuropathology, University Hospital Zurich, Zurich, Switzerland Affiliation Institute of Neuropathology, University Hospital Zurich, Zurich, Switzerland Affiliation Institute of Neuropathology, University Hospital Zurich, Zurich, Switzerland Unaltered Prion Pathogenesis in a Mouse Model of High-Fat Diet-Induced Insulin Resistance Epidemiological, clinical, and experimental animal studies suggest a strong correlation between insulin resistance and Alzheimers disease. In fact, type-2 diabetes is considered an important risk factor of developing Alzheimers disease. In addition, impaired insulin signaling in the Alzheimers disease brain may promote A production, impair A clearance and induce tau hyperphosphorylation, thereby leading to deterioration of the disease. The pathological prion protein, PrPSc, deposits in the form of extracellular aggregates and leads to dementia, raising the question as to whether prion pathogenesis may also be affected by insulin resistance. We therefore established high-fat diet-induced insulin resistance in tga20 mice, which overexpress the prion protein. We then inoculated the insulin-resistant mice with prions. We found that insulin resistance in tga20 mice did not affect prion disease progression, PrPSc deposition, astrogliosis or microglial activation, and had no effect on survival. Our study demonstrates that in a mouse model, insulin resistance does not significantly contribute to prion pathogenesis. Citation: Zhu C, Schwarz P, Abakumova I, Aguzzi A (2015) Unaltered Prion Pathogenesis in a Mouse Model of High-Fat Diet-Induced Insulin Re Continue reading >>
Calpain-10 Regulates Fat-induced Insulin Resistance
Calpain-10 Regulates Fat-Induced Insulin Resistance Genetic variation in the non-l Genetic variation in the non-lysosomal cysteine protease calpain-10 modifies risk of type 2 diabetes. However, the molecular basis for its effect on risk is unclear. In order to gain a better understanding of the effect of calpain-10 on glucose homeostasis, we generated a mouse model of calpain-10 deficiency by targeted gene disruption. The calpain-10 knockout (Capn10[sup]-/-)[/sup] mice develop normally and are fertile. They are about 10% smaller than wild-type littermates primarily due to a decrease in lean muscle mass. There is no significant difference in glucose tolerance (intraperitoneal glucose tolerance test), glucose-stimulated insulin secretion (perfused pancreas) and thermogenesis between Capn10[sup]-/-[/sup] and wild-type mice. The Capn10[sup]-/-[/sup] have significantly lower serum insulin levels compared to wild-type mice on both normal chow and high-fat diets. Euglycemic hyperinsulinemic clamp studies show that the Capn10[sup]-/-[/sup] mice are more insulin sensitive than wild-type littermates, especially on a high fat diet, and appear to be protected from diet-induced insulin resistance in skeletal muscle and liver. Calpain-10 is also abundantly expressed in the central nervous system (CNS). We have used a battery of behavioral tests to assess calpain-10 function in the CNS. The Capn10[sup]-/-[/sup] mice display normal balance and coordination and muscle strength but show significantly increased activity in an open field test. They display lower levels of anxiety-like behavior in the elevated plus maze and may have better memory (fear-conditioning test). Our results suggest that calpain-10 is an important factor contributing to fat-induced insulin resistance. Drugs target Continue reading >>
High-fructose And High-fat Diet-induced Insulin Resistance Enhances Atherosclerosis In Watanabe Heritable Hyperlipidemic Rabbits
High-fructose and high-fat diet-induced insulin resistance enhances atherosclerosis in Watanabe heritable hyperlipidemic rabbits Individuals with insulin resistance and resulting impaired glucose tolerance along with type 2 diabetes showed an increased prevalence of atherosclerosis. Our aim in this study was to address whether diet-induced insulin resistance plays any roles in the development of aortic and coronary atherosclerosis in hyperlipidemic rabbits. We fed Watanabe heritable hyperlipidemic (WHHL) rabbits with a high-fructose and high-fat diet (HFFD) with restricted normal calories and compared the lesions of both aortic and coronary atherosclerosis with those of control WHHL rabbits fed a normal chow diet. HFFD-fed WHHL rabbits showed insulin resistance and impaired glucose tolerance accompanied by elevated plasma lipid levels and accumulation of adipose tissue even though their body weight was unchanged compared to the control rabbits. At 8 weeks, the aortic gross lesion area of HFFD-fed WHHL rabbits was increased by 40 % over the controls and their lesions were characterized by increased number of macrophages and smooth muscle cells. At 16 weeks, the lesions of HFFD-fed WHHL rabbits showed more advanced lesions such as lipid core formation and calcification. In addition, coronary atherosclerosis was significantly increased in HFFD-fed WHHL rabbits. These results suggest that insulin resistance accelerates lesion formation of atherosclerosis. Insulin ResistanceCoronary AtherosclerosisCholesteryl Ester Transfer ProteinMicrosomal Triglyceride Transfer ProteinAdvanced Lesion Insulin resistance (IR) is frequently associated with many metabolic diseases such as obesity, hypertriglyceridemia, type 2 diabetes, and metabolic syndrome [ 1 ]. Individuals with underlying Continue reading >>
Pharmacological Tlr4 Inhibition Protects Against Acute And Chronic Fat-induced Insulin Resistance In Rats
Pharmacological TLR4 Inhibition Protects against Acute and Chronic Fat-Induced Insulin Resistance in Rats Affiliation Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, United States of America Affiliations Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, United States of America, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, United States of America, The Geriatric Research Education and Clinical Center, South Texas Veterans Health Care System, San Antonio, TX, 78229, United States of America Affiliations Department of Internal Medicine, The University of South Florida, Tampa, FL 33620, United States of America, James A Hayley Veterans Medical Center, Tampa, FL, 33612, United States of America Affiliations Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, United States of America, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, United States of America * E-mail: [email protected] (SHE); [email protected] (NM) Affiliations Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, United States of America, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, United States of America, The Geriatric Research Education and Clinical Center, South Texas Veterans Health Care System, San Antonio, TX, 78229, United States of America Continue reading >>
How Does Fat Affect Insulin Resistance And Diabetes?
According to the Centers for Disease Control, 29 million people in America have diabetes and 86 million have prediabetes. Insulin resistance is recognized as a predictor of type 2 diabetes, heart disease, and obesity. But what causes insulin resistance? In this NutritionFacts.org video, Dr. Michael Greger talks about how fat affects insulin resistance, and about how the most effective way to reduce insulin sensitivity is to reduce fat intake. We’ve also provided a summary of Dr. Greger’s main points below. Insulin Resistance of People on High-Fat Diets vs. High-Carb Diets In studies performed as early as the 1930s, scientists have noted a connection between diet and insulin intolerance. In one study, healthy young men were split into two groups. Half of the participants were put on a fat-rich diet, and the other half were put on a carb-rich diet. The high-fat group ate olive oil, butter, mayonnaise, and cream. The high-carb group ate pastries, sugar, candy, bread, baked potatoes, syrup, rice, and oatmeal. Within two days, tests showed that the glucose intolerance had skyrocketed in the group eating the high-fat diet. This group had twice the blood sugar levels than the high-carb group. The test results showed that the higher the fat content of the diet, the higher the blood sugar levels would be. What Is Insulin Resistance? It turns out that as the amount of fat in the diet goes up, so does one’s blood sugar spikes. Athletes frequently carb-load before a race because they’re trying to build up fuel in their muscles. We break down starch into glucose in our digestive tract; it circulates as blood glucose (blood sugar); and it is then used by our muscle cells as fuel. Blood sugar, though, is like a vampire. It needs an invitation to enter our cells. And that invit Continue reading >>
Prevention Of Fat-induced Insulin Resistance By Salicylate
Prevention of fat-induced insulin resistance by salicylate Jason K. Kim ,1,2 Yoon-Jung Kim ,2 Jonathan J. Fillmore ,2 Yan Chen ,1 Irene Moore ,2 Jongsoon Lee ,3 Minsheng Yuan ,3 Zhi Wei Li ,4 Michael Karin ,4 Pascale Perret ,2 Steven E. Shoelson ,3 and Gerald I. Shulman 1,2,5 1Howard Hughes Medical Institute,2Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA3Joslin Diabetes Center and the Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA4Department of Pharmacology, University of California, San Diego, School of Medicine, La Jolla, California, USA5Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut, USA 1Howard Hughes Medical Institute,2Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA3Joslin Diabetes Center and the Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA4Department of Pharmacology, University of California, San Diego, School of Medicine, La Jolla, California, USA5Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut, USA 1Howard Hughes Medical Institute,2Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA3Joslin Diabetes Center and the Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA4Department of Pharmacology, University of California, San Diego, School of Medicine, La Jolla, California, USA5Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut, USA 1Howard Hughes Medical Institute,2Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA3Joslin D Continue reading >>
What Causes Insulin Resistance? Lipid Overload
Over the past year I have interacted with hundreds of people with diabetes, and have come to learn one very important lesson that has changed my view of diabetes altogether. This realization came to me early on in my career as a nutrition and fitness coach for people with diabetes, and continues to hold true. While insulin resistance is a condition that is most commonly associated with type 2 diabetes, an increasing body of evidence is now shedding light on the fact that insulin resistance is a common thread that underlies many health conditions previously unassociated with blood sugar, including (but not limited to) heart disease, diabetes, atherosclerosis, the metabolic syndrome, obesity and cancer. What that means is simple: insulin resistance significantly increases your risk for the development of a collection of health conditions that can significantly reduce your quality of life and decrease your life expectancy. Watch this video for a synopsis of the causes of insulin resistance: What is insulin and why should you care? Insulin is a hormone which is released by the pancreas in response to rising blood glucose. When you consume carbohydrates, the glucose that enters the bloodstream knocks on the door of the beta cells in the pancreas as a signal to make insulin. Insulin serves as the key that unlocks the door to allow glucose to enter body tissues. Insulin tells your cells “Yoo hoo! Pick up this glucose. It’s all over the place.” Without insulin, cells in the liver, muscle, and fat have a difficult time vacuuming up glucose from the blood. These tissues are capable to vacuuming up only a small percentage (5-10%) of the glucose in circulation without the help of insulin. When insulin is present, the amount of glucose that can be transported into tissues sign Continue reading >>
Fat-induced Insulin Resistance And Atherosclerosis
Fat-Induced Insulin Resistance and Atherosclerosis Physiological elevations of plasma free fatty acid (FFA) levels cause peripheral (muscle), hepatic, and vascular insulin resistance, whereas lowering of plasma FFA levels improves peripheral insulin sensitivity in diabetic and nondiabetic subjects. FFA-induced insulin resistance in muscle is produced by defects in insulin-stimulated glucose transport and/or phosphorylation and in glycogen synthesis, which develop over 26 h. Development of these defects is temporally associated with accumulation in liver and in muscle cells of diacylglycerol (DAG) and activation of serine/threonine kinases including protein kinase C (PKC) and inhibitor of B-kinase. In nondiabetic, obese subjects, FFA-induced insulin resistance is fully or nearly fully compensated by FFA-mediated stimulation of insulin secretion. In patients with type 2 diabetes mellitus (T2DM), FFA-mediated stimulation of insulin secretion is impaired; hence, FFA-induced insulin resistance needs to be compensated by hype glycemia. Acute elevation of plasma FFA levels also activate the proinflammatory and proatherosclerotic inhibitor of B/nuclear factor B pathway in muscle and liver and this might play a role in the pathogenesis of atherosclerotic vascular disease and nonalcoholic fatty liver disease. Normalizing plasma FFA levels is, therefore, proposed as an approach to reduce insulin resistance and the risk for type 2 diabetes, atherosclerotic vascular diseases and nonalcoholic fatty liver disease. AtherosclerosisdiacylglycerolFFAhepatic andperipheral insulin resistanceinflammatory cytokinesinhibitor of B (IB) kinasenonalcoholic fatty liver diseasenuclear factorB pathwayprotein kinase Ctype 2 diabetes This is a preview of subscription content, log in to check access U Continue reading >>
