Comparison of ventromedial and paraventricular lesions in rats that become obese

Abstract

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.