King B M, Phelps G R, Frohman L A
Am J Physiol. 1980 Dec;239(6):E437-41. doi: 10.1152/ajpendo.1980.239.6.E437.
In order to assess the role of vagally mediated hyperinsulinemia in hypothalamic obesity, plasma insulin and glucose levels were assayed in vagotomized and sham-vagotomized female rats after a 6-h fast and after a measured glucose meal both before and 10-14 days after ventromedial hypothalamic (VMH) lesions. Both groups displayed similar gains in body weight in the first 10 days after VMH lesions, but only the sham-vagotomized VMH-lesioned animals displayed elevated fasting insulin levels. Fasting glucose levels did not differ either before or after the lesion. The insulin response to oral glucose was increased in VMH rats, both in vagotomized and sham-vagotomized animals, and it is concluded that the hyperresponsiveness to oral glucose is independent of vagal mediation. Vagotomy markedly exaggerated the glucose and insulin response to oral glucose loading in both intact rats and rats with VMH lesions, probably as a result of more rapid absorption of glucose from the intestine. It is concluded that the fasting hyperinsulinemia that is characteristic of VMH animals is under vagal control and that its elimination does not prevent the development of obesity.
为了评估迷走神经介导的高胰岛素血症在下丘脑性肥胖中的作用，在腹内侧下丘脑（VMH）损伤前及损伤后10 - 14天，对迷走神经切断和假迷走神经切断的雌性大鼠在禁食6小时后以及给予定量葡萄糖餐后，测定其血浆胰岛素和葡萄糖水平。两组在VMH损伤后的前10天体重增加相似，但只有假迷走神经切断的VMH损伤动物空腹胰岛素水平升高。损伤前后空腹血糖水平均无差异。VMH大鼠对口服葡萄糖的胰岛素反应增强，无论是迷走神经切断还是假迷走神经切断的动物都是如此，得出的结论是对口服葡萄糖的高反应性与迷走神经介导无关。迷走神经切断显著夸大了完整大鼠和VMH损伤大鼠对口服葡萄糖负荷的葡萄糖和胰岛素反应，这可能是由于葡萄糖从肠道吸收更快所致。得出的结论是，VMH动物特有的空腹高胰岛素血症受迷走神经控制，消除该症状并不能阻止肥胖的发展。
