Lakshmanan M R, Nepokroeff C M, Porter J W
Proc Natl Acad Sci U S A. 1972 Dec;69(12):3516-9. doi: 10.1073/pnas.69.12.3516.
The usual increase in the activity of liver fatty-acid synthetase that occurs on refeeding of a fat-free diet to previously fasted rats is abolished in diabetic animals. Insulin specifically restores this increase by enhancement of the rate of synthesis of fatty-acid synthetase. However, glucagon and cyclic AMP inhibit the increase in the activity of fatty-acid synthetase. Therefore, the concentration of fatty-acid synthetase in rat liver is under the control of the relative concentrations of insulin and glucagon.
给先前禁食的大鼠重新喂食无脂饮食后,肝脏脂肪酸合成酶活性通常会增加,但在糖尿病动物中这种增加被消除。胰岛素通过提高脂肪酸合成酶的合成速率特异性地恢复这种增加。然而,胰高血糖素和环磷酸腺苷抑制脂肪酸合成酶活性的增加。因此,大鼠肝脏中脂肪酸合成酶的浓度受胰岛素和胰高血糖素相对浓度的控制。