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High Fat Diet Insulin Resistance Mechanism

Insulin Sensitivity: The Secret To Optimal Health

Insulin Sensitivity: The Secret To Optimal Health

Insulin Sensitivity: The Secret to Optimal Health Insulin sensitivity is a vital mechanism in your body that determines how efficient your body utilizes the effects of insulin. People with low insulin sensitivity have a higher chance of developing metabolic diseases such as diabetes, obesity and heart disease. While some people may be born with healthier insulin sensitivity levels, there are several lifestyle changes you can make to improve it. The more insulin sensitive your body is, the more effective it is in utilizing carbohydrates for energy and the easier it becomes for your body to lose weight. Because of this, the weight loss industry has begun to magnify the importance of insulin sensitivity. Insulin is a crucial hormone secreted by your pancreas. Insulins job is to manage the nutrients you absorb from food. Insulin is known for its role in controlling blood sugar and carbohydrate consumption. When you eat carbs, it increases the level of blood sugar in your bloodstream. This is acknowledged by the cells in your pancreas which then releases insulin into the blood. Once the insulin is traveling in your bloodstream, it starts signaling the bodys cells that they should pick up sugar from the blood. The purpose of this cycle is to reduce the amount of sugar in your blood and place it where its supposed to, into cells for storage. This is crucial because abnormally high amounts of sugar in your blood can have harmful effects to your body and in some cases can lead to death if neglected. Insulin sensitivity is a system in the body that determines how effectively your body can utilize carbohydrates. Insulin sensitivity arbitrates how much insulin your body needs to produce to precipitate a certain amount of glucose (sugar). Its the mechanism in your body that determi 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 >>

High-fat Load: Mechanism(s) Of Insulin Resistance In Skeletal Muscle

High-fat Load: Mechanism(s) Of Insulin Resistance In Skeletal Muscle

High-fat load: mechanism(s) of insulin resistance in skeletal muscle We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. High-fat load: mechanism(s) of insulin resistance in skeletal muscle D S Lark, K H Fisher-Wellman, and P D Neufer Skeletal muscle from sedentary obese patients is characterized by depressed electron transport activity, reduced expression of genes required for oxidative metabolism, altered mitochondrial morphology and lower overall mitochondrial content. These findings imply that obesity, or more likely the metabolic imbalance that causes obesity, leads to a progressive decline in mitochondrial function, eventually culminating in mitochondrial dissolution or mitoptosis. A decrease in the sensitivity of skeletal muscle to insulin represents one of the earliest maladies associated with high dietary fat intake and weight gain. Considerable evidence has accumulated to suggest that the cytosolic ectopic accumulation of fatty acid metabolites, including diacylglycerol and ceramides, underlies the development of insulin resistance in skeletal muscle. However, an alternative mechanism has recently been evolving, which places the etiology of insulin resistance in the context of cellular/mitochondrial bioenergetics and redox systems biology. Overnutrition, particularly from high-fat diets, generates fuel overload within the mitochondria, resulting in the accumulation of partially oxidized acylcarnitines, increased mitochondr Continue reading >>

High-fat Diets Cause Insulin Resistance Despite An Increase In Muscle Mitochondria

High-fat Diets Cause Insulin Resistance Despite An Increase In Muscle Mitochondria

High-fat diets cause insulin resistance despite an increase in muscle mitochondria We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. High-fat diets cause insulin resistance despite an increase in muscle mitochondria Chad R. Hancock, Dong-Ho Han, [...], and John O. Holloszy It has been hypothesized that insulin resistance is mediated by a deficiency of mitochondria in skeletal muscle. In keeping with this hypothesis, high-fat diets that cause insulin resistance have been reported to result in a decrease in muscle mitochondria. In contrast, we found that feeding rats high-fat diets that cause muscle insulin resistance results in a concomitant gradual increase in muscle mitochondria. This adaptation appears to be mediated by activation of peroxisome proliferator-activated receptor (PPAR) by fatty acids, which results in a gradual, posttranscriptionally regulated increase in PPAR coactivator 1 (PGC-1) protein expression. Similarly, overexpression of PPAR results in a large increase in PGC-1 protein in the absence of any increase in PGC-1 mRNA. We interpret our findings as evidence that raising free fatty acids results in an increase in mitochondria by activating PPAR, which mediates a posttranscriptional increase in PGC-1. Our findings argue against the concept that insulin resistance is mediated by a deficiency of muscle mitochondria. Keywords: mitochondrial biogenesis, mitochondrial dysfunction, PPAR, skeletal muscle, PGC-1 It has b Continue reading >>

High-fat Diet Induces Hepatic Insulin Resistance And Impairment Of Synaptic Plasticity

High-fat Diet Induces Hepatic Insulin Resistance And Impairment Of Synaptic Plasticity

High-Fat Diet Induces Hepatic Insulin Resistance and Impairment of Synaptic Plasticity Zhigang Liu , Ishan Y. Patil , Tianyi Jiang , Harsh Sancheti , John P. Walsh , Bangyan L. Stiles , Fei Yin , Enrique Cadenas Affiliations: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America, College of Food Science and Engineering, Northwest A&F University, Yangling, China Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Davis School of Gerontology and Program in Neuroscience, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America High-fat diet (HFD)-induced obesity is associated with insulin resistance, which may affect brain synaptic plasticity through impairment of insulin-sensitive processes underlying neuronal survival, learning, and memory. The experimental model consis Continue reading >>

Variability In Myosteatosis And Insulin Resistance Induced By High-fat Diet In Mouse Skeletal Muscles

Variability In Myosteatosis And Insulin Resistance Induced By High-fat Diet In Mouse Skeletal Muscles

Variability in Myosteatosis and Insulin Resistance Induced by High-Fat Diet in Mouse Skeletal Muscles 1Department of Drug Science and Technology, University of Turin, Via Giuria 9, 10125 Turin, Italy 2Department of Clinical and Biological Sciences, University of Turin, Corso Raffaello 30, 10125 Turin, Italy 3Department of Molecular Medicine University of Pavia, Via Forlanini 6, 27100 Pavia, Italy 4Division of Endocrinology, Diabetology and Metabolism, Department of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126 Turin, Italy Received 29 May 2014; Accepted 28 July 2014; Published 14 August 2014 Copyright 2014 Massimo Collino et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Nutrient overload leads to impaired muscle oxidative capacity and insulin sensitivity. However, comparative analyses of the effects of dietary manipulation on skeletal muscles with different fiber composition are lacking. This study aimed to investigate the selective adaptations in the soleus and tibialis anterior muscles evoked by administration of high-fat diet for 12 weeks in 10 mice (HFD mice) compared to 10 animals fed with a normal chow diet (control mice). Mice fed with the HFD diet exhibited hyperlipidemia, hyperinsulinemia, hyperglycemia, and lower exercise capacity in comparison to control mice. In control mice, soleus fibers showed higher lipid content than tibialis anterior fibers. In contrast, the lipid content was similar between the two muscles in HFD mice. Significant differences in markers of muscle mitochondrial production and/or activity as well as of lipid synthesis were detected between HFD mi Continue reading >>

Exercise Improved Lipid Metabolism And Insulin Sensitivity In Rats Fed A High-fat Diet By Regulating Glucose Transporter 4 (glut4) And Musclin Expression

Exercise Improved Lipid Metabolism And Insulin Sensitivity In Rats Fed A High-fat Diet By Regulating Glucose Transporter 4 (glut4) And Musclin Expression

Braz J Med Biol Resvol.49no.5Ribeiro Preto2016 EpubApr29, 2016 Exercise improved lipid metabolism and insulin sensitivity in rats fed a high-fat diet by regulating glucose transporter 4 (GLUT4) and musclin expression 1Department of Endocrinology, The First Hospital of Jiujiang City, Jiangxi Province, China Jiujiang Affiliated Hospital of Nanchang University, Jiujiang, Jiangxi Province, China This study aimed to evaluate the effects of exercise training on triglyceride deposition and the expression of musclin and glucose transporter 4 (GLUT4) in a rat model of insulin resistance. Thirty male Sprague-Dawley rats (8 weeks old, weight 16010 g) were fed a high-fat diet (40% calories from fat) and randomly divided into high-fat control group and swimming intervention group. Rats fed with standard food served as normal control. We found that 8-week swimming intervention significantly decreased body weight (from 516.2346.27 to 455.4332.55 g) and visceral fat content (from 39.362.50 to 33.022.24 g) but increased insulin sensitivity index of the rats fed with a high-fat diet. Moreover, swimming intervention improved serum levels of TG (from 1.400.83 to 0.580.26 mmol/L) and free fatty acids (from 837.80164.25 to 556.38144.77 Eq/L) as well as muscle triglycerides deposition (from 0.550.06 to 0.450.02 mmol/g) in rats fed a high-fat diet. Compared with rats fed a standard food, musclin expression was significantly elevated, while GLUT4 expression was decreased in the muscles of rats fed a high-fat diet. In sharp contrast, swimming intervention significantly reduced the expression of musclin and increased the expression of GLUT4 in the muscles of rats fed a high-fat diet. In conclusion, increased musclin expression may be associated with insulin resistance in skeletal muscle, and exe Continue reading >>

Mechanism By Which Dietary Fat Can Raise Blood Glucose And Insulin

Mechanism By Which Dietary Fat Can Raise Blood Glucose And Insulin

Mechanism By Which Dietary Fat Can Raise Blood Glucose And Insulin Back in 2008 , I began writing about the effect of dietary fat on insulin sensitivity, and blood levels of glucose and insulin. Heres one of the studies: It was a small randomized crossover study on healthy subjects that compared: High-fat diet (40% carbohydrate, 45% fat) High-carb diet (55% carbohydrate, 30% fat) During the oral-glucose-tolerance test, both glucose and insulin rose to higher concentrations after the high-fat diet than after the high-carb diet, showing lower glucose tolerance and insulin sensitivity with the high-fat diet. Over the years I learned that saturated fat decreased insulin sensitivity more than other fats, e.g. the KANWU Study . One mechanism by which dietary fat decreases insulin sensitivity, raising blood glucose and insulin levels is through reduced action of the glucose transporter GLUT4. There seems to be both a reduced expression of the GLUT4 gene, and a reduced translocation or movement of GLUT4 to the cell membrane in the presence of a high-fat, especially high-saturated fat diet. (GLUT4 is one of the glucose transport proteins that move glucose from the bloodstream into muscle and fat cells. Its insertion into the membrane is controlled by insulin. See diagram.) When glucose cannot enter cells, blood glucose levels rise. When normal amounts of insulin fail to clear blood of glucose, the pancreas responds by releasing more. The result is impaired glucose tolerance, hyperinsulinemia, and eventual development of type 2 diabetes. Over time, compensatory insulin output from beta cells in the pancreas diminishes and a person with type 2 diabetes may find themselves injecting insulin instead of just taking oral meds. Here are some studies and reviews that address this: 1. A Continue reading >>

Frontiers | Skeletal Muscle Mitochondrial Bioenergetics And Morphology In High Fat Diet Induced Obesity And Insulin Resistance: Focus On Dietary Fat Source | Physiology

Frontiers | Skeletal Muscle Mitochondrial Bioenergetics And Morphology In High Fat Diet Induced Obesity And Insulin Resistance: Focus On Dietary Fat Source | Physiology

Front. Physiol., 20 January 2016 | Skeletal Muscle Mitochondrial Bioenergetics and Morphology in High Fat Diet Induced Obesity and Insulin Resistance: Focus on Dietary Fat Source Department of Biology, University of Naples Federico II, Naples, Italy It has been suggested that skeletal muscle mitochondria play a key role in high fat (HF) diet induced insulin resistance (IR). Two opposite views are debated on mechanisms by which mitochondrial function could be involved in skeletal muscle IR. In one theory, mitochondrial dysfunction is suggested to cause intramyocellular lipid accumulation leading to IR. In the second theory, excess fuel within mitochondria in the absence of increased energy demand stimulates mitochondrial oxidant production and emission, ultimately leading to the development of IR. Noteworthy, mitochondrial bioenergetics is strictly associated with the maintenance of normal mitochondrial morphology by maintaining the balance between the fusion and fission processes. A shift toward mitochondrial fission with reduction of fusion protein, mainly mitofusin 2, has been associated with reduced insulin sensitivity and inflammation in obesity and IR development. However, dietary fat source during chronic overfeeding differently affects mitochondrial morphology. Saturated fatty acids induce skeletal muscle IR and inflammation associated with fission phenotype, whereas -3 polyunsaturated fatty acids improve skeletal muscle insulin sensitivity and inflammation, associated with a shift toward mitochondrial fusion phenotype. The present minireview focuses on mitochondrial bioenergetics and morphology in skeletal muscle IR, with particular attention to the effect of different dietary fat sources on skeletal muscle mitochondria morphology and fusion/fission balance. Sk Continue reading >>

High Fat Diet Induces Central Obesity, Insulin Resistance And Microvascular Dysfunction In Hamsters

High Fat Diet Induces Central Obesity, Insulin Resistance And Microvascular Dysfunction In Hamsters

Volume 82, Issue 3 , November 2011, Pages 416-422 High fat diet induces central obesity, insulin resistance and microvascular dysfunction in hamsters Microvascular dysfunction is an early finding in obesity possibly related to co-morbidities like diabetes and hypertension. Therefore we have investigated changes on microvascular function, body composition, glucose and insulin tolerance tests (GTT and ITT) on male hamsters fed either with high fat (HFD, n=20) or standard (Control, n=21) diet during 16weeks. Total body fat and protein content were determined by carcass analysis, aorta eNOS and iNOS expression by immunoblotting assay and mean blood pressure (MAP) and heart rate (HR) by an arterial catheter. Microvascular reactivity in response to acetylcholine and sodium nitroprusside, functional capillary density (FCD), capillary recruitment induced by a hyperinsulinemic status and macromolecular permeability after 30min ischemia was assessed on either cheek pouch or cremaster muscle preparations. Compared to Control, HFD animals have shown increased visceral fat (6.00.8 vs. 13.80.6g/100g BW), impaired endothelial dependent vasodilatation, decreased FCD (11.31.3 vs. 6.81.2/field) and capillary recruitment during hyperinsulinemia and increased macromolecular permeability after ischemia/reperfusion (86.45.2 vs.105.25.1leaks/cm2), iNOS expression and insulin resistance. MAP, HR, endothelial independent vasodilatation and eNOS expression were not different between groups. Our results have shown that HFD elicits an increase on visceral fat deposition, microvascular dysfunction and insulin resistance in hamsters. We have studied microcirculatory effects of high fat diet in hamsters High fat diet blunted arteriolar response to acetylcholine and induced iNOS expression in aorta. 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 >>

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 >>

Cellular Mechanism By Which Estradiol Protects Female Ovariectomized Mice From High-fat Diet-induced Hepatic And Muscle Insulin Resistance

Cellular Mechanism By Which Estradiol Protects Female Ovariectomized Mice From High-fat Diet-induced Hepatic And Muscle Insulin Resistance

Cellular Mechanism by Which Estradiol Protects Female Ovariectomized Mice From High-Fat Diet-Induced Hepatic and Muscle Insulin Resistance Department of Internal Medicine (J.P.G.C., F.R.J., H.-Y.L., S.K., B.A.G., M.K., V.T.S., K.F.P., M.J.J., G.I.S.), New Haven, Connecticut 06536-9812 Department of Physiology and Biophysics (J.P.G.C., C.R.O.C.), Institute of Biomedical Sciences, University of So Paulo, 05508-900 So Paulo, Brazil Search for other works by this author on: Department of Internal Medicine (J.P.G.C., F.R.J., H.-Y.L., S.K., B.A.G., M.K., V.T.S., K.F.P., M.J.J., G.I.S.), New Haven, Connecticut 06536-9812 Search for other works by this author on: Department of Internal Medicine (J.P.G.C., F.R.J., H.-Y.L., S.K., B.A.G., M.K., V.T.S., K.F.P., M.J.J., G.I.S.), New Haven, Connecticut 06536-9812 Howard Hughes Medical Institute (H.-Y.L., G.I.S.), Yale University School of Medicine, New Haven, Connecticut 06536-9812 Search for other works by this author on: Department of Internal Medicine (J.P.G.C., F.R.J., H.-Y.L., S.K., B.A.G., M.K., V.T.S., K.F.P., M.J.J., G.I.S.), New Haven, Connecticut 06536-9812 Search for other works by this author on: Department of Internal Medicine (J.P.G.C., F.R.J., H.-Y.L., S.K., B.A.G., M.K., V.T.S., K.F.P., M.J.J., G.I.S.), New Haven, Connecticut 06536-9812 Search for other works by this author on: Department of Internal Medicine (J.P.G.C., F.R.J., H.-Y.L., S.K., B.A.G., M.K., V.T.S., K.F.P., M.J.J., G.I.S.), New Haven, Connecticut 06536-9812 Search for other works by this author on: Department of Internal Medicine (J.P.G.C., F.R.J., H.-Y.L., S.K., B.A.G., M.K., V.T.S., K.F.P., M.J.J., G.I.S.), New Haven, Connecticut 06536-9812 Search for other works by this author on: Department of Physiology and Biophysics (J.P.G.C., C.R.O.C.), Institu Continue reading >>

The Mechanism Of Cetp-mediated Protection From High-fat Diet-induced Insulin Resistance Palmisano, Brian T. Vanderbilt University Medical Center, Nashville, Tn, United States

The Mechanism Of Cetp-mediated Protection From High-fat Diet-induced Insulin Resistance Palmisano, Brian T. Vanderbilt University Medical Center, Nashville, Tn, United States

The Mechanism of Cetp-Mediated Protection from High-Fat Diet-Induced Insulin Resistance Obesity causes insulin resistance, which increases the risk of Type 2 Diabetes (T2D) and Coronary Heart Disease (CHD). Although weight loss is a primary goal in clinical management of obesity, long-term weight loss is rarely sustained. Therefore, it is imperative to understand pathways that might ameliorate the impact of obesity on T2D and CHD. We discovered that transgenic expression of Cholesteryl Ester Transfer Protein (Cetp) protects against high-fat diet (HFD)-induced insulin resistance in female mice in the setting of obesity. Cetp traffics triglyceride and cholesteryl ester (CE) between plasma lipoproteins, culminating in delivery of CE to the liver for secretion as bile - termed reverse cholesterol transport (RCT). Cetp inhibitors raise high- density lipoprotein (HDL) but fail to reduce risk for CHD, which may indicate that Cetp has non-HDL functions. Mice lack Cetp, so we used transgenic mice expressing Cetp to define how Cetp impacts insulin resistance. Using the hyperinsulinemic-euglycemic clamp technique, we found that Cetp protects against insulin resistance in females, but not males following 4 weeks of HFD. This protection was despite a similar degree of obesity. The objective of this proposal is to understand how Cetp protects against insulin resistance in diet-induced obese mice. Our discovery represents a novel and beneficial function of Cetp with regard to obesity pathophysiology. Despite high-fat feeding, Cetp expression preserved insulin signaling pathways in liver and muscle and insulin-mediated downregulation of mRNA for gluconeogenic genes Phosphoenopyruvate Carboxykinase (Pck1) and Glucose-6-Phosphatase (G6pc). We found that Cetp increased mRNA of the bile a 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 >>

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