Stricker E M, McCann M J
Brain Res Bull. 1985 Jun;14(6):687-92. doi: 10.1016/0361-9230(85)90119-4.
Some years ago, we reported that the increased blood intake of hypoglycemic rats was inhibited by the intravenous infusion of fructose, a sugar that cannot cross the blood-brain barrier and nourish cerebral chemoreceptors. More recent experiments therefore have focused on visceral factors in the control of food intake. Three observations have been emphasized in this review. First, we found that gastric emptying was increased during insulin-induced hypoglycemia, and that this effect also was eliminated by administration of fructose. Hepatic vagotomy abolished both this effect of fructose on gastric emptying and its effect on food intake. Second, we found that in rats with severe diabetes, the rate of gastric emptying did decrease in proportion to increasing concentration of an administered glucose load, as it does in intact rats, but calories emptied more rapidly than normal regardless of the concentration of the load. Third, we found that rats with varying degrees of streptozotocin-induced damage to the pancreas ate more food than intact rats did after an overnight fast, and that individual intakes were proportional to the induced glucose intolerance. The increased eating took the form of shorter intermeal intervals, as if the initial postfast meal did not remain satiating for a normal amount of time. These and other findings suggest that food intake is controlled in part by satiety signals apparently related to the delivery of utilizable calories plus insulin to the liver. These signals also seem to affect gastric emptying and thereby might influence other satiety signals related to gastric distention.
几年前，我们报告说，果糖静脉输注可抑制低血糖大鼠增加的摄食量，果糖是一种无法穿过血脑屏障并滋养脑化学感受器的糖。因此，最近的实验集中在食物摄入控制中的内脏因素上。本综述强调了三项观察结果。首先，我们发现胰岛素诱导的低血糖期间胃排空增加，并且果糖给药也消除了这种作用。肝迷走神经切断术消除了果糖对胃排空的这种作用及其对食物摄入的作用。其次，我们发现，在患有严重糖尿病的大鼠中，胃排空率确实与所给予的葡萄糖负荷浓度增加成比例地降低，就像在完整大鼠中一样，但无论负荷浓度如何，卡路里排空都比正常情况更快。第三，我们发现，在禁食过夜后，不同程度链脲佐菌素诱导的胰腺损伤的大鼠比完整大鼠吃更多的食物，并且个体摄入量与诱导的葡萄糖不耐受成比例。进食增加表现为餐间间隔缩短，就好像禁食后的第一餐在正常时间内没有保持饱腹感一样。这些以及其他发现表明，食物摄入部分受饱腹感信号控制，这些信号显然与可利用卡路里加胰岛素向肝脏的输送有关。这些信号似乎也会影响胃排空，从而可能影响与胃扩张相关的其他饱腹感信号。
