Parameswaran S V, Steffens A B, Hervey G R, de Ruiter L
Am J Physiol. 1977 May;232(5):R150-7. doi: 10.1152/ajpregu.1977.232.5.R150.
Excessive food intake and obesity was induced in one member of parabiotic pairs by electrical stimulation (three 30-min sessions/day for 2 wk) of the lateral hypothalamus (LH). The nonstimulated partners reduced spontaneous food intake the fatter the stimulated animals became. This reduced food intake resulted in a decreased body weight, fat content, and fat-free solid body mass. The decrease of food intake was not due to changed social behavior of the obese partner. It must be attributed to transmission of a humoral satiety factor. The very first stimulation of the LH in the stimulated partners resulted in a large increase in blood glucose and glucagon level without much change in the insulin level. These changes in blood parameters were probably due to strong sympathetic arousal. In the nonstimulated animals there were practically no changes in these parameters. One week of fattening resulted in increased basal glucose and insulin levels in the stimulated animals and decreased glucose levels in the nonstimulated partners, in which the basal insulin levels remained nearly normal. Basal glucagon levels were the same in both partners and did not differ from the prefattening situation. At that time during stimulation the obese animals showed a large increase in glucose and glucagon levels and a decrease in insulin level. On the other hand the nonstimulated animals showed a slow gradual increase in glucose and insulin level due to transmission from their fat partners because of the large gradient in these substances between the animals. These phenomena were still more pronounced after 2 wk of fattening. It is tentatively concluded that the humoral satiety factor is neither circulating insulin nor glucagon nor one of the major circulating nutrients.
通过对联体动物对中的一只进行下丘脑外侧区(LH)电刺激(每天3次,每次30分钟,持续2周)来诱导其过度进食和肥胖。随着受刺激动物变得越胖,未受刺激的伙伴自发进食量减少。这种进食量的减少导致体重、脂肪含量和去脂固体体重下降。进食量的减少并非由于肥胖伙伴社交行为的改变。这一定归因于一种体液性饱腹感因子的传递。对受刺激伙伴的LH进行首次刺激后,血糖和胰高血糖素水平大幅升高,而胰岛素水平变化不大。这些血液参数的变化可能是由于强烈的交感神经兴奋。在未受刺激的动物中,这些参数几乎没有变化。一周的育肥导致受刺激动物的基础血糖和胰岛素水平升高,而未受刺激伙伴的血糖水平下降,其基础胰岛素水平几乎保持正常。两个伙伴的基础胰高血糖素水平相同,与育肥前的情况没有差异。在刺激期间,肥胖动物的血糖和胰高血糖素水平大幅升高,胰岛素水平下降。另一方面,未受刺激的动物由于其肥胖伙伴体内这些物质的巨大梯度传递,血糖和胰岛素水平缓慢逐渐升高。育肥2周后,这些现象更加明显。初步得出结论,体液性饱腹感因子既不是循环胰岛素,也不是胰高血糖素,也不是主要的循环营养素之一。