diabetestalk.net

Fat Induced Insulin Resistance

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

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 >>

High-fat Diet-induced Insulin Resistance In Single Skeletal Muscle Fibers Is Fiber Type Selective

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 >>

Calpain-10 Regulates Fat-induced Insulin Resistance

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 >>

Prevention Of Fat-induced Insulin Resistance By Salicylate

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 >>

P24sucrose- And High Fat-induced Insulin Resistance Leads To Endothelial Dysfunction And Is Associated With Ketohexokinase Activation | Heart

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 >>

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

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 >>

Prevention Of Fat-induced Insulin Resistance By Salicylate.

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 >>

Mechanisms Of Fatty Acid-induced Insulin Resistance In Muscle And Liver

Mechanisms Of Fatty Acid-induced Insulin Resistance In Muscle And Liver

1University of Ain Shams – Department of Biochemistry – Faculty of Science, Cairo – Egypt 2University Health Network, Canada 3Hospital for Sick Children, Canada 4Mount Sinai Hospital, Canada 5University of Toronto, Toronto, Canada Corresponding Author: Rafik Ragheb University of Toronto, Toronto – Canada Tel/Fax: 1-905-2099660 E-mail: [email protected] Citation: Ragheb R, Medhat AM (2011) Mechanisms of Fatty Acid-Induced Insulin Resistance in Muscle and Liver. J Diabetes Metab 2:127. doi:10.4172/2155-6156.1000127 Copyright: © 2011 Ragheb R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Abstract Insulin Resistance occurs as a result of disturbances in lipid metabolism and increased levels of circulating fatty acids that accumulate within the insulin sensitive tissues such as muscle, liver and adipose tissues. Increased fatty acid flux has been suggested to be strongly associated with insulin resistant states such as obesity and type 2-diabetes. Fatty acids appear to cause this defect in glucose transport by inhibiting insulin -stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and reducing IRS-1 associated phosphatidyl-inositol 3-kinase activity that implicate other insulin signaling components downstream of the insulin signaling cascade. A number of different metabolic abnormalities may increase intramyocellular or intrahepatic fatty acid metabolites that induce the disease state of insulin resistance through a number of different cellular mechanisms. The current review 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

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 >>

Low Dose Fat-induced Insulin Resistance

Low Dose Fat-induced Insulin Resistance

You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details. ClinicalTrials.gov Identifier: NCT03479671 Recruitment Status : Not yet recruiting Information provided by (Responsible Party): Study Description Study Design Arms and Interventions Outcome Measures Eligibility Criteria Contacts and Locations More Information The primary goal of this study is to determine the dose of fatty acids that acutely induces mild insulin resistance in healthy volunteers. We hypothesize that a low-dose of fatty acid infusion (Intralipid/heparin) will cause a mild insulin resistance. The dose of fatty acid infusion that reliably causes mild insulin resistance will be selected for use in future studies. Diabetes Mellitus, Type 2 Insulin Resistance Insulin Sensitivity Drug: Intralipid, 20% Intravenous Emulsion This study is designed to test the hypothesis that a low-dose of fatty acid infusion (Intralipid/heparin) will cause mild insulin resistance. This dose-finding study is critical for future studies on free-fatty acid induced insulin resistance. Healthy male and healthy female volunteers will undergo a 6 hour hyperinsulinemic-euglycemic clamp, in order to establish insulin sensitivity parameters in the presence of fatty acid co-infusion. The subjects will then return 1-3 weeks later, and undergo another 6 hour HIE clamp, this time in the presence of low-dose fatty acid co-infusion (30ml/hr). I Continue reading >>

What Causes Insulin Resistance? Lipid Overload

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 >>

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

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 >>

Insulin Resistance

Insulin Resistance

Insulin resistance (IR) is a pathological condition in which cells fail to respond normally to the hormone insulin. The body produces insulin when glucose starts to be released into the bloodstream from the digestion of carbohydrates in the diet. Normally this insulin response triggers glucose being taken into body cells, to be used for energy, and inhibits the body from using fat for energy. The concentration of glucose in the blood decreases as a result, staying within the normal range even when a large amount of carbohydrates is consumed. When the body produces insulin under conditions of insulin resistance, the cells are resistant to the insulin and are unable to use it as effectively, leading to high blood sugar. Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level. This often remains undetected and can contribute to the development of type 2 diabetes or latent autoimmune diabetes of adults.[1] Although this type of chronic insulin resistance is harmful, during acute illness it is actually a well-evolved protective mechanism. Recent investigations have revealed that insulin resistance helps to conserve the brain's glucose supply by preventing muscles from taking up excessive glucose.[2] In theory, insulin resistance should even be strengthened under harsh metabolic conditions such as pregnancy, during which the expanding fetal brain demands more glucose. People who develop type 2 diabetes usually pass through earlier stages of insulin resistance and prediabetes, although those often go undiagnosed. Insulin resistance is a syndrome (a set of signs and symptoms) resulting from reduced insulin activity; it is also part of a larger constellation of symptoms called the metabolic syndrome. Insuli Continue reading >>

Review Article Exercise And Obesity-induced Insulin Resistance In Skeletal Muscle

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 >>

How Does Fat Affect Insulin Resistance And Diabetes?

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 >>

More in ketosis