Is the effect of high fat diet on lipid and carbohydrate metabolism related to inflammation?

  title={Is the effect of high fat diet on lipid and carbohydrate metabolism related to inflammation?},
  author={Islam Ahmed Abd El-Hamid Ibrahim and Mona Fouad Mahmoud Abd El-Aziz and Ahmed F Ahmed and Mohamed Abd El-Aal Mohamed},
  journal={Mediterranean Journal of Nutrition and Metabolism},
Obesity is an emerging health problem in world wide countries. High fat diet (HFD), which is the main cause of obesity, induces inflammation and affects both lipid and carbohydrate metabolism. This study investigates the effect of inflammation induced by HFD on lipid and carbohydrate metabolism. This study involves two parts, in vivo and in vitro. In the in vivo part, adult male albino rats were fed a HFD for 8 and 14 weeks. After each feeding period, the following parameters were measured… 

High-fat diet effects on metabolic responses to chronic stress

High proportion of unsaturated fat may not lead to deleterious metabolic responses; however combined with chronic stress has a synergistic and adverse effect on visceral adiposity and results in elevated plasma leptin.



[Effect of high-fat diet, rosiglitazone on lipid profile, insulin resistance and liver steatosis development].

High-fat diet promotes the development of unfavorable lipid profile changes (hypercholesterolemia, hypertriglyceridemia), insulin resistance, as well as theDevelopment of liver steatosis, while rosiglitazone exerts a favorable effect on both lipid profile and regulation of insulin secretion, but it does not reduce the risk of liver Steatosis.

Relationship of dietary fat to glucose metabolism.

A High Fat Diet Impairs Stimulation of Glucose Transport in Muscle

Evidence is provided that impairment of muscle glucose transport by 8 weeks of high fat feeding is not due to plasma membrane composition-related reductions in glucose transporter or insulin receptor function, and a defect in insulin receptor signaling is a late event, not a primary cause, of the muscle insulin resistance induced by fat feeding.

Diet-Induced Muscle Insulin Resistance in Rats Is Ameliorated by Acute Dietary Lipid Withdrawal or a Single Bout of Exercise: Parallel Relationship Between Insulin Stimulation of Glucose Uptake and Suppression of Long-Chain Fatty Acyl-CoA

It is concluded that muscle insulin resistance induced by high-fat feeding is readily ameliorated by three independent, short-term physiological manipulations.

The Fatty Acid Receptor GPR40 Plays a Role in Insulin Secretion In Vivo After High-Fat Feeding

GPR40 plays a role not only in fatty acid modulation of insulin secretion, but also in GSIS after high-fat feeding, which raises doubts on the validity of a therapeutic approach based on GPR40 antagonism for the treatment of type 2 diabetes.

Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake.

It is demonstrated that the development of insulin resistance and type 2 diabetes during prolonged high-fat feeding are linked to the excess AGEs/advanced lipoxidation end products inherent in fatty diets.

Influence of Dietary Fat Composition on Development of Insulin Resistance in Rats: Relationship to Muscle Triglyceride and ω-3 Fatty Acids in Muscle Phospholipid

It is concluded that the particular fatty acids and the lipid environment in which they are presented in high-fat diets determine insulin sensitivity in rats and impaired insulin action in skeletal muscle relates to triglyceride accumulation, suggesting intracellular glucose–fatty acid cycle involvement.

Suppression of GLUT4 expression in skeletal muscle of rats that are obese from high fat feeding but not from high carbohydrate feeding or genetic obesity.

Obesity due to high fat feeding, but not that due toHigh calorie/carbohydrate feeding or genetics, is associated with pretranslational suppression of GLUT4 expression in skeletal muscle, demonstrating tissue-specific regulation of expression ofGLUT4 and GLUT1.

Increased oxidative stress in obesity and its impact on metabolic syndrome.

It is suggested that increased oxidative stress in accumulated fat is an early instigator of metabolic syndrome and that the redox state in adipose tissue is a potentially useful therapeutic target for obesity-associated metabolic syndrome.