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Related Experiment Videos

Cholate inhibits high-fat diet-induced hyperglycemia and obesity with acyl-CoA synthetase mRNA decrease

S Ikemoto1, M Takahashi, N Tsunoda

  • 1Division of Clinical Nutrition, National Institute of Health and Nutrition, Tokyo, Japan.

The American Journal of Physiology
|July 1, 1997
PubMed
Summary
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Sodium cholate prevents high-fat diet-induced hyperglycemia and obesity by improving insulin sensitivity and reducing liver triglyceride accumulation. This bile acid may offer a novel therapeutic strategy for metabolic disorders.

Area of Science:

  • Biochemistry
  • Metabolic Physiology
  • Nutritional Science

Background:

  • High-fat diets induce hyperglycemia and obesity, leading to insulin resistance.
  • Bile acids play a role in lipid and glucose metabolism.
  • Understanding mechanisms to counteract diet-induced metabolic dysfunction is crucial.

Purpose of the Study:

  • To investigate the effects of sodium cholate on high-fat diet-induced hyperglycemia and obesity.
  • To elucidate the molecular mechanisms underlying cholate's metabolic effects.

Main Methods:

  • C57BL/6J mice were fed a high-safflower oil diet with or without 0.5% sodium cholate.
  • Insulin resistance was assessed by measuring 2-deoxyglucose uptake in epitrochlearis muscles.
  • Liver and muscle tissue analyses were performed to evaluate lipid accumulation and gene expression.

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Main Results:

  • Sodium cholate completely prevented high-fat diet-induced hyperglycemia and obesity.
  • Cholate improved glucose uptake in muscles and decreased blood insulin levels.
  • Cholate prevented liver triglyceride accumulation and downregulated acyl-CoA synthetase (ACS) mRNA levels.

Conclusions:

  • Sodium cholate exhibits protective effects against diet-induced metabolic disorders.
  • The benefits of cholate may be partly mediated by the downregulation of ACS mRNA in the liver.
  • Sodium cholate represents a potential therapeutic agent for managing obesity and hyperglycemia.