Involvement of a humoral factor in regulation of body weight in parabiotic rats
Parameswaran, S.V.; Steffens, A.B.; Hervey, G.R.; de Ruiter, L.
American Journal of Physiology 232(5): R150-R157
1977
ISSN/ISBN: 0002-9513 PMID: 324294 Document Number: 120750
Excessive food intake and obesity were induced in one member of parabiotic pairs of rats by electrical stimulation (three 30-min sessions/day for 2 weeks) of the lateral hypothalamus (LH). The nonstimulated partners reduced spontaneous food intake the fatter the stimulated animals became; reduced intake resulted in decreased bodyweight, fat content and fat-free solid body mass. The decrease of food intake was not due to changed social behaviour of the obese partner. It must be attributed to transmission of a humoral satiety factor. The first stimulation of the LH in the stimulated partners resulted in a large increase in blood glucose and glucagon without much change in insulin, probably due to strong sympathetic arousal. In the nonstimulated animals there was practically no change in these values. One week of fattening resulted in increased basal glucose and insulin in the stimulated and decreased glucose in the nonstimulated partners, in which the basal insulin remained nearly normal. Basal glucagon values were the same in both partners and did not differ from those before fattening. At that time during stimulation the obese animals showed a large increase in glucose and glucagon and a decrease in insulin. The nonstimulated animals showed a slow gradual increase in glucose and insulin due to transmission from their fat partners because of the large gradient in these substances between the animals. Those phenomena were still more pronounced after 2 weeks of fattening. It is tentatively concluded that the humoral satiety factor is not circulating insulin nor glucagon nor one of the major circulating nutrients.