Goodman M W, Prigge W F, Gebhard R L
Am J Physiol. 1981 Apr;240(4):G274-80. doi: 10.1152/ajpgi.1981.240.4.G274.
Hormonal regulation of intestinal cholesterol synthesis was studied both in vitro and in vivo. Cholesterol synthesis rate was determined by measurement of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (EC 1.1.1.34) activity and by incorporation [14C]acetate into sterol. In vitro studies utilized organ culture of canine ileal mucosa. During 6-h culture, reductase activity was stimulated sevenfold. Insulin (10-6 M) augmented this rise to 144 +/- 7% of th control activity, while 10(-8) M glucagon, 10(-3) M adenosine 3',5'-cyclic monophosphate, and 3-isobutyl-1-methylxanthine suppressed activity (final reductase activity was 83 +/- 3%, 75 +/- 4%, and 41 +/- 3%, respectively, of cultured control values). In vivo studies utilized dogs with isolated Thiry-Vella ileal fistulas. In vivo, insulin doubled reductase activity while glucagon led to a 42 +/- 9% suppression. It is concluded that insulin and glucagon may be potential physiological regulators of intestinal cholesterol synthesis. The glucagon effect may be mediated by cyclic nucleotides.
对肠道胆固醇合成的激素调节进行了体外和体内研究。通过测量3-羟基-3-甲基戊二酰辅酶A还原酶（EC 1.1.1.34）的活性以及将[14C]乙酸盐掺入甾醇中来确定胆固醇合成速率。体外研究采用犬回肠粘膜的器官培养。在6小时培养期间，还原酶活性增加了7倍。胰岛素（10-6 M）使这种升高增加到对照活性的144±7%，而10（-8）M胰高血糖素、10（-3）M腺苷3',5'-环磷酸和3-异丁基-1-甲基黄嘌呤抑制活性（最终还原酶活性分别为培养对照值的83±3%、75±4%和41±3%）。体内研究采用具有孤立的Thiry-Vella回肠瘘的犬。在体内，胰岛素使还原酶活性加倍，而胰高血糖素导致42±9%的抑制。结论是胰岛素和胰高血糖素可能是肠道胆固醇合成的潜在生理调节剂。胰高血糖素的作用可能由环核苷酸介导。
