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Glucagon and Glucocorticoids in the Regulation of Rat Liver Cystathionine Synthetase Activity

Department of Biochemistry and the Kohlberg Laboratory, National Defense Medical Center; and Medical Research Laboratory, Veterans General Hospital Taipei, Taiwan, Republic of China

Send reprint requests to Foo Pan, Department of Biochemistry, National Defense Medical Center, P. O. Box 7432, Taipei, Taiwan, Republic of China.

Abstract

The characteristics of the induction of hepatic cystathionine synthetase by glucagon have been studied in male rats. Administration of glucagon to intact rats caused a significant increase in the synthetase level within 12 hr. The minimum effective dose tested was 12.5 µg and the optimal dose was about 25 µg/100 g of body weight, given subcutaneously every 6 hr. The nutritional status of the animals has a profound influence upon the effectiveness of exogenous glucagon on this enzyme. Although the response of cystathionine synthetase to glucagon was reduced, it was not abolished by adrenalectomy. A combined treatment with glucagon and cortisone acetate brought about a much greater response than either treatment alone in both intact and adrenalectomized rats. The data indicate that different mechanisms account for the increase in this enzyme caused by glucagon or adrenal glucocorticoids. This conclusion is further supported by the evidence that starvation exerts different effects on the response of the synthetase to glucagon or cortisone. The enhancement of hepatic cystathionine synthetase activity by glucagon was blocked by simultaneous administration of cycloheximide, actinomycin D or aflatoxin B₁. The effect of triamcinolone was also prevented by actinomycin D. The results suggest that the rise in cystathionine synthetase activity mediated by glucagon and glucocorticoids involves the formation of new RNA and the synthesis of new protein. (Endocrinology 88: 723, 1971)

Received August 6, 1970.