Abstract

Bilateral electrolytic lesions in the ventromedial hypothalamic nuclei (VMN) were produced in two groups of weanling male rats. Two groups of rats received lesions in the dorsomedial hypothalamic nuclei (DMN). Six days later, one of the VMN groups received DMN lesions (VMN and DMN), while VMN lesions were produced in one of the DMN groups (DMN and VMN). Sham-operated animals served as controls. The animals were maintained for 18 days during which time food intake was measured. On the 19th day they were decapitated and the following parameters determined: carcass fat, plasma insulin, glucose, triglyceride and cholesterol, and body weight and length. DMN lesions failed to attenuate the ‘principal’ parameters of the weanling rat ventromedial syndrome: hyperinsulinemia, hyperlipidemia and increased carcass fat. This was irrespective of the sequence of the two hypothalamic operations. Food intake, body weight and length proved amenable to DMN lesions only when DMN were produced prior to VMN lesions, but it is noteworthy that in these animals plasma insulin and lipid levels remained elevated despite a reduced food intake. Neither of the groups with double lesions had glucose values which were significantly different from those of the controls. The data point to a profound autonomy of the ventromedial hypothalamic nuclei and their related circuits in the development of the weanling rat VMN syndrome.

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