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

Am J Physiol. 1997 Jul;273(1 Pt 1):E37-45. doi: 10.1152/ajpendo.1997.273.1.E37.

Abstract

The effects of sodium cholate on high-fat diet-induced hyperglycemia and obesity were investigated. Insulin resistance was estimated by measuring 2-deoxyglucose uptake in epitrochlearis muscles incubated in vitro. Addition of 0.5% cholate to high-safflower oil diet completely prevented high fat-induced hyperglycemia and obesity in C57BL/6J mice with a slight decrease of energy intake but with no inhibition of fat absorption. Furthermore, the addition of cholate decreased blood insulin levels and prevented high-fat diet-induced decrease of glucose uptake in epitrochlearis. However, there was no change in the unsaturation index of fatty acids in skeletal muscles and in GLUT-4 levels by cholate. In liver, cholate addition resulted in cholesterol accumulation and completely prevented high-fat diet-induced triglyceride accumulation. The changes of triglyceride level in the liver were paralleled to the changes of acyl-CoA synthetase (ACS) mRNA. ACS catalyzes the formation of acyl-CoA from fatty acid, and acyl-CoA is utilized for triglyceride formation in liver. ACS has a sterol-responsive element 1 in its promoter region. These data indicate that the favorable effects of cholate could be partly the result of downregulation of ACS mRNA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Cholesterol / metabolism
  • Cholic Acid
  • Cholic Acids / pharmacology*
  • Coenzyme A Ligases / biosynthesis*
  • Dietary Fats* / analysis
  • Energy Intake
  • Fatty Acids / analysis
  • Fatty Acids / chemistry
  • Fatty Acids, Nonesterified / metabolism
  • Feces / chemistry
  • Female
  • Gene Expression Regulation, Enzymologic / drug effects
  • Glucose Transporter Type 4
  • Hyperglycemia / etiology
  • Hyperglycemia / prevention & control*
  • Liver / drug effects
  • Liver / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Monosaccharide Transport Proteins / metabolism
  • Muscle Proteins*
  • Muscle, Skeletal / drug effects
  • Muscle, Skeletal / metabolism
  • Obesity / enzymology
  • Obesity / etiology
  • Obesity / prevention & control*
  • Phospholipids / chemistry
  • RNA, Messenger / biosynthesis*
  • Repressor Proteins*
  • Saccharomyces cerevisiae Proteins*
  • Transcription, Genetic / drug effects*
  • Triglycerides / metabolism

Substances

  • Cholic Acids
  • Dietary Fats
  • Fatty Acids
  • Fatty Acids, Nonesterified
  • Glucose Transporter Type 4
  • Monosaccharide Transport Proteins
  • Muscle Proteins
  • Phospholipids
  • RNA, Messenger
  • Repressor Proteins
  • Saccharomyces cerevisiae Proteins
  • Slc2a4 protein, mouse
  • Triglycerides
  • Cholesterol
  • Coenzyme A Ligases
  • FAA2 protein, S cerevisiae
  • long-chain-fatty-acid-CoA ligase
  • Cholic Acid