scholarly journals High-fat diet, muscular lipotoxicity and insulin resistance

2007 ◽  
Vol 66 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Patrick Schrauwen
Keyword(s):  
Physical Activity ◽  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mitochondrial Function ◽  
Dietary Fat ◽  
Plasma Fatty Acid ◽  
Fat Intake ◽  
High Fat

A high dietary fat intake and low physical activity characterize the current Western lifestyle. Dietary fatty acids do not stimulate their own oxidation and a surplus of fat is stored in white adipose tissue, liver, heart and muscle. In these organs intracellular lipids serve as a rapidly-available energy source during, for example, physical activity. However, under conditions of elevated plasma fatty acid levels and high dietary fat intake, conditions implicated in the development of modern diseases such as obesity and type 2 diabetes mellitus, fat accumulation in liver and muscle (intramyocellular lipids; IMCL) is associated with the development of insulin resistance. Recent data suggest that IMCL are specifically harmful when combined with reduced mitochondrial function, both conditions that characterize type 2 diabetes. In the (pre)diabetic state reduced expression of the transcription factor PPARγ co-activator-1α (PGC-1α), which is involved in mitochondrial biogenesis, has been suggested to underlie the reduced mitochondrial function. Importantly, the reduction in PGC-1α may be a result of low physical activity, consumption of high-fat diets and high plasma fatty acid levels. Mitochondrial function can also be impaired as a result of enhanced mitochondrial damage by reactive oxygen species. Fatty acids in the vicinity of mitochondria are particularly prone to lipid peroxidation. In turn, lipid peroxides can induce oxidative damage to mitochondrial RNA, DNA and proteins. The mitochondrial protein uncoupling protein 3, which is induced under high-fat conditions, may serve to protect mitochondria against lipid-induced oxidative damage, but is reduced in the prediabetic state. Thus, muscular lipotoxicity may impair mitochondrial function and may be central to insulin resistance and type 2 diabetes mellitus.

1734-P: High Dietary Fat Intake Exacerbates Insulin Resistance in a Type 2 Diabetes Genetic Mouse Model

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1734-P
Author(s):  
AUSTIN REILLY ◽  
SHIJUN YAN ◽  
ALEXA J. LONCHARICH ◽  
HONGXIA REN
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mouse Model ◽  
Dietary Fat ◽  
Fat Intake ◽  
Dietary Fat Intake ◽  
Genetic Mouse Model

scholarly journals Establishment of long-term high-fat diet and low dose streptozotocin-induced experimental type-2 diabetes mellitus model of insulin resistance and evaluation of seed extracts of Syzygium cumini

2021 ◽  
Vol 10 (3) ◽  
pp. 331-338
Author(s):  
Pratibha Nadig ◽  
Meharban Asanaliyar ◽  
Kevin Manohar Salis
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
High Fat Diet ◽  
Low Dose ◽  
Syzygium Cumini ◽  
High Fat ◽  
Glut 4 ◽  
Seed Extracts

Introduction: The principal mechanism responsible for reducing blood glucose is through insulin-stimulated glucose transport into skeletal muscle. The transporter protein that mediates this uptake is GLUT-4. A defect in this step is associated with reduced glucose utilization in muscle and adipose tissue, as observed in insulin-resistant type-2 diabetes mellitus (T2DM) patients. This study aimed to develop an experimental T2DM model and evaluate altered glucose transporter type 4 (GLUT-4) levels as a biomarker of insulin resistance. Antidiabetic activities of Syzygium cumini hydro-ethanolic seed extracts (SCE) were also evaluated. Methods: Adult male Wistar albino rats were fed a high-fat diet for 12 weeks and dosed intraperitoneally with streptozotocin (35 mg/kg). After treatment for 21 days, all investigations were done. The homeostasis model of assessment (HOMA) was used for the calculation of insulin resistance (HOMA-IR) and beta-cell function (HOMA-B) index. Diaphragm muscle and retroperitoneal fat were collected for real-time polymerase chain reaction (RT-PCR) studies. Results: A significant increase in fasting blood glucose, HOMA-IR, and serum lipids, and a decrease in serum insulin and HOMA-B were observed in the diabetic group, effects that reversed following pioglitazone and SCE treatment. The diabetic group showed a downregulation of GLUT-4 expression in skeletal muscle while an increase was observed in adipose tissue. Conclusion: A high-fat diet and low dose streptozotocin-induced experimental T2DM model of insulin resistance was developed to screen novel insulin sensitizers. Data generated demonstrated that altered GLUT-4 levels could be used as a biomarker of insulin resistance. Antidiabetic activity of S. cumini hydro-ethanolic seed extract was also confirmed in this study.

The Role of Diet in Patients with Metabolic Syndrome

2019 ◽  
Vol 26 (19) ◽  
pp. 3613-3619 ◽  
Author(s):  
Paloma Almeda-Valdes ◽  
Roberto J. Herrera-Mercadillo ◽  
Carlos A. Aguilar-Salinas ◽  
Misael Uribe ◽  
Nahum Méndez-Sánchez
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Coronary Heart Disease ◽  
Dietary Fat ◽  
Lifestyle Modification ◽  
Fat Intake ◽  
High Prevalence

Metabolic syndrome is a frequent metabolic disorder characterized by obesity and insulin resistance seems to be the main pathophysiological alteration. The goal of treating metabolic syndrome is to reduce the risk of coronary heart disease and the development of type 2 diabetes. The lifestyle modification therapy combines specific recommendations on diet alone or combined with other strategies. In this review, we address the following topics: 1) the importance of the high prevalence of metabolic syndrome and obesity, and 2) the role of lifestyle modification focusing on dietary fat intake in the management of MS.

scholarly journals Total and subtypes of dietary fat intake and risk of type 2 diabetes mellitus in the Prevención con Dieta Mediterránea (PREDIMED) study

2017 ◽  
Vol 105 (3) ◽  
pp. 723-735 ◽  
Author(s):  
Marta Guasch-Ferré ◽  
Nerea Becerra-Tomás ◽  
Miguel Ruiz-Canela ◽  
Dolores Corella ◽  
Helmut Schröder ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Dietary Fat ◽  
Fat Intake ◽  
Dietary Fat Intake ◽  
Predimed Study ◽  
Dieta Mediterranea ◽  
Dieta Mediterránea

scholarly journals Low-carbohydrate and high-fat intake among adult patients with poorly controlled type 2 diabetes mellitus

Nutrition ◽  
2006 ◽  
Vol 22 (11-12) ◽  
pp. 1129-1136 ◽  
Author(s):  
Yunsheng Ma ◽  
Barbara C. Olendzki ◽  
Andrea R. Hafner ◽  
David E. Chiriboga ◽  
Annie L. Culver ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Adult Patients ◽  
Fat Intake ◽  
High Fat ◽  
Low Carbohydrate

Differences in the interaction between CETP Taq1B polymorphism and dietary fat intake on lipid profile of normolipedemic and dyslipidemic patients with type 2 diabetes mellitus

2018 ◽  
Vol 37 (1) ◽  
pp. 270-275 ◽  
Author(s):  
Zahra Kalantar ◽  
Mohamad Reza Eshraghian ◽  
Gity Sotoudeh ◽  
Mahmoud Djalali ◽  
Anahita Mansouri ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Lipid Profile ◽  
Dietary Fat ◽  
Fat Intake ◽  
Dietary Fat Intake

Abstract P130: Risk Factors for Progression to Type 2 Diabetes Mellitus From Prediabetes

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Margareta Hellgren ◽  
Ulf Lindblad ◽  
Bledar Daka
Keyword(s):  
Physical Activity ◽  
Diabetes Mellitus ◽  
Risk Factors ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Family History ◽  
Glucose Tolerance

Background and Aims: Individuals with prediabetes, impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT), have approximately 50% risk to develop type 2 diabetes mellitus (T2DM) within ten years. This paper examines risk factors for development of T2DM in individuals with prediabetes. Materials and Methods: A total of 2816 individuals were randomly selected and completed a careful physical examination and an oral glucose tolerance test. IFG and IGT was defined according to WHO. A representative sample of 1327 individuals were re-examined in a follow-up study after ten years. This study focuses on the participants who were diagnosed with prediabetes, IFG (n=67) and/or IGT (n=89) at baseline and who were re-examined at follow-up. Insulin resistance was estimated by HOMA-ir (Homeostatic Model Assessment for Insulin Resistance). Differences between the participants with prediabetes who developed T2DM and those who did not, were analyzed with general linear models and adjusted for age, sex and BMI. The risk to progress to T2DM in ten years was explored using binary logistic regression, adding the risk-factors one after another. Results: Of the 156 individuals with prediabetes 28% progressed to T2DM. Individuals who developed T2DM had higher BMI (α=3.2kg/m 2 , P<0.001), higher HbA1c (α=0.2 mmol/mol, P=0.047), higher C-reactive protein (α=3.3 mmol/L, P=0.040) and also significantly higher HOMAir (α=2.8, P<0.001) at base-line. The risk to develop T2DM increased in a step-wise manner in individuals with prediabetes when successively adding the risk-factors. Having a BMI ≥30kg/m 2 , a known family history for T2DM, HbA1c ≥37mmol/mol, HOMAir ≥2.8 and a low level of physical activity increased the risk to develop T2DM 5.6 times. Table 1. Conclusion: In individuals with prediabetes, those with additional risk-factors like obesity, HbA1c and HOMAir above mean values, family history for T2DM and a low level of physical activity require extra attention and intensive lifestyle interventions should be initiated.

scholarly journals Hypermethylation of Hepatic Glucokinase and L-Type Pyruvate Kinase Promoters in High-Fat Diet–Induced Obese Rats

Endocrinology ◽  
2011 ◽  
Vol 152 (4) ◽  
pp. 1284-1289 ◽  
Author(s):  
Minghong Jiang ◽  
Yuhao Zhang ◽  
Meng Liu ◽  
Michael Shihli Lan ◽  
Jing Fei ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Dna Methylation ◽  
Type 2 Diabetes Mellitus ◽  
High Fat Diet ◽  
High Fat ◽  
Dna Hypermethylation ◽  
Obese Rats

Abstract Obesity-dependent insulin resistance and type 2 diabetes mellitus are closely associated with decreased glucose utilization and down-regulation of hepatic glycolytic enzymes expression. Previously, we showed that DNA hypermethylation is involved in age-dependent susceptibility to hepatic insulin resistance and diabetes. However, what we cannot distinguish is whether the age-related obesity contributes to DNA hypermethylation in those natural aging rats. In the present study, we hypothesize that DNA methylation plays a crucial role in the regulation of glycolytic enzymes in the high-fat diet–induced obesity. Here, we report that DNA hypermethylation is correlated with a decline in hepatic glucokinase (Gck) and L-type pyruvate kinase (LPK) expression in high-fat diet–induced obese rats as compared with the control diet group. Down-regulation of Gck and LPK expression are reversed by the 5-aza-2′-deoxycytidine in the cell model of steatosis. These novel observations indicate that DNA methylation is involved in the development of metabolic diseases, such as obesity, insulin resistance, type 2 diabetes mellitus, and nonalcoholic steatohepatitis, suggesting that the hypermethylation level of Gck and LPK promoters may be a useful parameter for the evaluation of obesity-induced insulin resistance and fatty liver.

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