Friedman M I, Granneman J
Am J Physiol. 1983 Mar;244(3):R374-82. doi: 10.1152/ajpregu.1983.244.3.R374.
Rats increased food intake after plasma glucose returned to normal in the wake of an insulin-induced hypoglycemic episode. Whereas increased eating 6-8 h after insulin occurred only when plasma glucose levels fell below 70 mg/dl, intakes were not related to the degree of prior hypoglycemia. Administration of glucose in the first 3 h after insulin prevented increased eating, whereas glucose given 4-6 h after insulin was less effective. Intravenous infusions of fructose given in the first 3 h after insulin injection prevented increased food intake in normal but not hepatic-vagotomized rats. Determination of various metabolic variables in parallel experiments showed that insulin treatment resulted in changes in peripheral metabolism, which persisted at the time feeding tests were conducted, and that administration of glucose or fructose tended to reverse these changes. The results suggest that increased food intake after recovery from hypoglycemia is associated with peripheral metabolic consequences of ongoing or previous counterregulatory responses which occur during hypoglycemia and that alterations in hepatic metabolism are sufficient to inhibit this insulin-induced eating.
在胰岛素诱导的低血糖发作后,当血浆葡萄糖恢复正常时,大鼠的食物摄入量增加。虽然仅在血浆葡萄糖水平降至70mg/dl以下时,胰岛素注射后6 - 8小时才会出现进食增加,但摄入量与先前低血糖的程度无关。在胰岛素注射后的前3小时给予葡萄糖可防止进食增加,而在胰岛素注射后4 - 6小时给予葡萄糖的效果较差。在胰岛素注射后的前3小时静脉输注果糖可防止正常大鼠进食增加,但对肝迷走神经切断的大鼠无效。在平行实验中对各种代谢变量的测定表明,胰岛素治疗导致外周代谢发生变化,在进行喂食试验时这些变化仍然存在,并且给予葡萄糖或果糖倾向于逆转这些变化。结果表明,低血糖恢复后的食物摄入量增加与低血糖期间发生的持续或先前的反调节反应的外周代谢后果有关,并且肝脏代谢的改变足以抑制这种胰岛素诱导的进食。