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

Shinji Ikemoto, Mayumi Takahashi, Nobuyo Tsunoda, Kayo Maruyama, Hiroshige Itakura, Kentaro Kawanaka, Izumi Tabata, Mitsuru Higuchi, Tsuyoshi Tange, Tokuo T. Yamamoto, Osamu Ezaki*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

71 Citations (Scopus)


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.

Original languageEnglish
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Issue number1 36-1
Publication statusPublished - 1997 Jul
Externally publishedYes


  • Cholesterol
  • Desaturase
  • Glucose uptake
  • Insulin resistance
  • Triglyceride

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Biochemistry
  • Physiology (medical)


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