Lesions in the ventromedial hypothalamus (VMH) uniformly produced obesity, but lesions in the paraventricular nucleus (PVN) produced obesity in only half of the animals. The obesity in the PVN-lesioned animals was related to the extent of PVN damage and was attenuated by concurrent damage to the dorsomedial nucleus. Comparing the PVN-lesioned rats that became obese with the VMH-lesioned rats that showed comparable weight gain, revealed several differences. The nocturnal intake of food in rats eating ad libitum was lower in the VMH-lesioned rats. Glucose concentrations were also lower in the VMH-lesioned rats, whether eating ad libitum or pair fed. Insulin concentrations were higher in the fatter animals fed ad libitum regardless of the location of the lesion. After pair feeding the insulin values were lower in both VMH- and PVN-lesioned rats than in controls. The diurnal excursion of corticosterone was blunted by both hypothalamic lesions in rats fed ad libitum, but after pair feeding there was less distortion of the diurnal rhythm. These data show that the characteristics of obesity produced by PVN lesions differ from those resulting from VMH damage.
The effects of vagotomy on plasma glucose and insulin levels in rats with paraventricular nuclear (PVN) or ventromedial hypothalamic (VMH) lesions were measured during a constant glucose infusion. In one experiment, vagotomy was performed 50 min after the lesions, and in a second experiment, it was performed at the same time as the lesions. After the introduction of lesions in the PVN, there was a significantly greater rise in plasma glucose than in animals with either large or small VMH lesions, both of which had plasma glucose values similar to those in the sham-lesioned animals. The rise in insulin was greater in all three lesion groups than in the sham-operated animals. Although both plasma glucose and insulin had begun to decline before the vagotomy performed 50 min after lesioning, there was a further subsequent fall after vagotomy which was greater in the VMH-lesioned animals with large lesions than in rats with PVN lesions or small VMH lesions. In the sham-lesioned rats, there was no significant change in insulin or glucose after vagotomy. When the vagotomy and hypothalamic lesions were performed simultaneously, the glucose and insulin values in all groups were the same. The present experiments suggest that VMH and PVN exert different controls over pancreatic hormone secretion. The VMH lesions appear to remove an inhibitory effect on the vagus, with resultant hyperinsulinemia in the absence of hyperglycemia. The PVN-lesioned animals show a hyperglycemia which is abolished by vagotomy, suggesting that the PVN connects to vagal fibers which activate the glucagon secretory system in the alpha-cell of the pancreas.
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