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Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
08:13

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

Published on: January 7, 2018

Toll-like receptor 2-deficient mice are protected from insulin resistance and beta cell dysfunction induced by a

J A Ehses1, D T Meier, S Wueest

  • 1Department of Surgery, Faculty of Medicine, University of British Columbia, Child & Family Research Institute, 950 W 28th Ave, Vancouver, BC, Canada V5Z 4H4. ehses@interchange.ubc.ca

Diabetologia
|April 22, 2010
PubMed
Abstract

Insights

Toll-like receptor 2 (TLR2) plays a role in high-fat diet-induced metabolic dysfunction. Mice lacking TLR2 were protected from diet-induced insulin resistance and inflammation, suggesting TLR2 as a therapeutic target.

Area of Science:

  • Metabolic disease research
  • Immunology
  • Endocrinology

Background:

  • Inflammation is a key factor in type 2 diabetes, contributing to insulin resistance and pancreatic beta-cell dysfunction.
  • Toll-like receptors (TLRs) are crucial in innate immunity, recognizing substances like non-esterified fatty acids (NEFAs) and initiating inflammatory responses.

Purpose of the Study:

  • To investigate the role of Toll-like receptor 2 (TLR2) in metabolic disturbances caused by high-fat diet (HFD) feeding in mice.
  • To determine if TLR2 contributes to diet-induced insulin resistance and inflammation.

Main Methods:

  • Comparative analysis of glucose tolerance, insulin sensitivity, insulin secretion, and energy metabolism in Tlr2(+/+) and Tlr2(-/-) mice on chow and HFD.
  • Molecular examination of adipose, liver, muscle, and islet tissues for pathology and inflammation.
  • In vitro assessment of NEFA-induced cytokine production in macrophages, dendritic cells, and pancreatic islets.

Main Results:

  • Tlr2(-/-) mice were protected from HFD-induced adverse metabolic effects, unlike Tlr2(+/+) controls.
  • Female Tlr2(-/-) mice exhibited significant improvements in glucose tolerance, insulin sensitivity, and secretion after HFD.
  • Protection correlated with enhanced fat utilization and reduced tissue inflammation in Tlr2(-/-) mice, with diminished IL-1beta response to NEFAs.

Conclusions:

  • TLR2 acts as a molecular mediator linking high dietary lipid intake to glucose homeostasis.
  • TLR2 influences glucose regulation through its control over energy substrate utilization and tissue inflammation.

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