Insulin Sensitivity and Carbohydrate Metabolism of Rats With Hypothalamic Obesity

Abstract

SUMMARY A fixed dose of glucose, irrespective of body weight, used for i.v. glucose tolerance tests in rats with hypothalamic obesity and in non-obese control rats caused almost identical blood glucose increments in both kinds of rats, and the K values (coefficients of glucose assimilation) were not significantly different. Glucose doses proportional to body weight caused much larger increments of blood glucose in the obese animals but the K value was not significantly different from that for the controls. On the other hand, the insulin sensitivity of obese rats was found to be less than that of control rats when a fixed dose of the hormone was given. When the insulin dosage was proportional to body weight, the fall of fasting blood glucose produced in the obese animals was not significantly different from that in the control group. In vitro, the diaphragm muscle of the obese animals was insensitive to the action of insulin as compared with controls. There was no evidence of insulin insensitivity of the obese animals' adipose tissue; the very low metabolic activity of the adipose tissue of both the control and obese animals may have been responsible. The interpretation of these findings is discussed in the light of similar work in human obesity.

Organization of projections from the ventromedial nucleus of the hypothalamus: A Phaseolus vulgaris‐Leucoagglutinin study in the rat

“…Thus, apart from regulating food intake, the VMH may also play a role in diet-induced thermogenesis by influencing sympathetic drive to brown adipose tissue (Perkins et al, 1981;Niijima et al, 1984;Holt et al, 1987;Le Feuvre et al, 1991). In addition, the VMH may influence 1) the secretion of insulin and glucagon; 2 ) hepatic glucose production, peripheral glucose utilization, and free fatty acid mobilization (Hales and Kennedy, 1964;Tucker et al, 1964;Frohman and Bernardis, 1971;Goldman et al, 1972;Takahashi and Shirnazu, 1981); and 3) gastric secretion (Ridley and Brooks, 1965;Costal1 et al, 1986;Gunion and Tache, 1987;Gunion et al, 1990).…”

The Effect of a High-Carbohydrate Diet on Glucose, Insulin Sensitivity and Plasma Insulin in Rats

“…Apart from peripheral factors which can inhibit the action of insulin on the uptake of glucose in animals fed on a high-sucrose diet, there are other circumstances at cell level which antagonize the action of the hormone. Tissues incubated in vitro (Tucker, Trethewey, Stewart, Neville & Hanley, 1965) were also found to be less sensitive to the action of the insulin. Increased ingestion of sucrose by our rats caused an increase in plasma glucose with subsequent increase in glycogen deposits.…”

Adrenal medullary function and expression of catecholamine-synthesizing enzymes in mice with hypothalamic obesity

“…The hypothalamus plays a pivotal role in the control of food intake and energy homeostasis (Woods et al, 1985;Lawrence et al, 1999;Schwartz et al, 2000). The destruction of specific hypothalamic centers leads to the classically defined hypothalamic obesity (Tucker et al, 1965;Bray et al, 1981). Neonatal administration of monosodium glutamate (MSG) produces lesions in arcuate nucleus and median eminence of hypothalamus (McBride et al, 1976;Leigh et al, 1992).…”