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Am J Physiol Endocrinol Metab 273: E37-E45, 1997;
0193-1849/97 $5.00
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AJP - Endocrinology and Metabolism, Vol 273, Issue 1 E37-E45, Copyright © 1997 by American Physiological Society

ARTICLES

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

S. Ikemoto, M. Takahashi, N. Tsunoda, K. Maruyama, H. Itakura, K. Kawanaka, I. Tabata, M. Higuchi, T. Tange, T. T. Yamamoto and O. Ezaki
Division of Clinical Nutrition, National Institute of Health and Nutrition, Tokyo, Japan.

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.


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