Acute hyperinsulinemia and its reversal by vagotomy after lesions of the ventromedial hypothalamus in anesthetized rats.
The acute effect of bilateral electrolytic ventromedial hypothalamic lesions (20-25-m Coulomb stainless steel electrodes) on plasma levels of insulin and glucose was studied in anesthetized rats to determine early effects that would occur before hyperphagia and obesity. In rats fed ad libitum, lesions in the ventromedial hypothalamus (VMH) but not in the cortex produced a marked increase in circulating insulin levels (starting at 20 min postlesion) and a small increase in glycemia which, however, was not significant and could therefore not be the cause of increased insulin secretion. Hyperinsulinemia after VMH lesions was more pronounced when glucose was infused iv at a rate of 7-8 mg/kg . min. Bilateral subdiaphragmatic vagotomy, performed 50 min after VMH lesions, immediately and completely reversed the observed hyperinsulinemia. With the exception of a tendency of lesions producing the highest degree of hyperinsulinemia to be slightly larger than the lesions not producing any hyperinsulinemia, no statement about the critical involvement of a specific hypothalamic locus can be made. It is concluded that electrolytic VMH destruction causes immediate hypersecretion of the pancreatic B cell, an effect that requires the integrity of the vagus nerves. Further localization of the central circuitry responsible for this mechanism, however, will require more specific methods than electrolytic lesions.
D000818:Animals; D001786:Blood Glucose; D006946:Hyperinsulinism / Q000209:etiology* / Q000503:physiopathology / Q000601:surgery; D007031:Hypothalamus / Q000503:physiopathology*; D007033:Hypothalamus, Middle / Q000503:physiopathology*; D007328:Insulin / Q000097:blood*; D008297:Male; D051381:Rats; D014628:Vagotomy; D014630:Vagus Nerve / Q000503:physiopathology*
D001786:Blood Glucose; D007328:Insulin