McCann M J, Stricker E M
Am J Physiol. 1986 Sep;251(3 Pt 2):R609-13. doi: 10.1152/ajpregu.1986.251.3.R609.
Previous work has established that the increased food intake of rats in response to insulin-induced hypoglycemia can be inhibited by the intravenous infusion of fructose, a sugar that cannot cross the blood-brain barrier and nourish cerebral chemoreceptors, and that this effect of fructose is abolished by hepatic vagotomy. The present series of experiments examined the effects of these treatments on gastric emptying of various glucose solutions in rats. Gastric emptying of the administered loads decreased in proportion to increasing concentration of glucose solution but not by enough for caloric delivery to be regulated precisely. Insulin-induced hypoglycemia increased the rate at which the glucose solutions emptied from the stomach. This enhanced emptying was suppressed by infusion of fructose, and that suppression was eliminated by hepatic vagotomy. These and other findings support previous proposals that food intake is controlled in part by satiety signals reflecting the nutrient content of the stomach and in part by satiety signals related to the delivery of utilizable calories to the liver.
先前的研究已经证实,静脉输注果糖可抑制大鼠因胰岛素诱导的低血糖而增加的食物摄入量。果糖是一种无法穿过血脑屏障并滋养脑化学感受器的糖类,并且果糖的这种作用可通过肝迷走神经切断术消除。本系列实验研究了这些处理对大鼠各种葡萄糖溶液胃排空的影响。所给予负荷的胃排空速率随着葡萄糖溶液浓度的增加而成比例降低,但降低幅度不足以精确调节热量输送。胰岛素诱导的低血糖增加了葡萄糖溶液从胃中排空的速率。输注果糖可抑制这种增强的排空,而肝迷走神经切断术可消除这种抑制作用。这些以及其他发现支持了先前的观点,即食物摄入量部分受反映胃中营养成分的饱腹感信号控制,部分受与可利用热量输送到肝脏相关的饱腹感信号控制。