Document Type

Article

Publication Date

1-1983

Department

Psychology

Abstract

The nature of and neural mechanisms involved in GH and insulin responses to obesity-inducing ventromedial hypothalamic (VMH) lesions, which infringed on the arcuate nucleus, were examined in freely moving chronically cannulated male rats. Sequential 6-h GH and 3-h insulin and glucose secretory profiles were obtained in VMH-lesioned and sham-operated control rats. Obese VMH rats exhibited hyperinsulinemia with marked fluctuations in plasma insulin levels in the presence of normoglycemia. A striking suppression in both amplitude and duration of GH secretory episodes was observed, with GH peak amplitudes rarely exceeding 90 ng/ml compared to 500 ng/ml in sham-operated controls (mean 6-h plasma GH level, 17.6 ± 6.0 vs. 154.1 ± 17.8 ng/ml; P < 0.001). The periodicity of the GH rhythm was maintained, but light-dark entrainment of the GH pulses was lost. Passive immunization with a specific antiserum to somatostatin (SRIF) failed to restore the amplitude of the GH peaks or to alter significantly the 6-h GH secretory profile of VMH-lesioned animals. In contrast, the administration of SRIF antiserum to sham-operated controls caused a significant elevation of GH trough levels. In a second study, obese VMHl-esioned rats exhibited reduced pituitary GH concentrations compared to sham-operated controls. The finding of a lack of effect of SRIF antiserum in VMHl-esioned rats provides good evidence that the suppression of GH pulses observed in response to lesions of the VMH is due to interruption of stimulatory pathways involved in GH regulation, namely GH-releasing factor neurons. The results suggest that the ultradian surges of GH release are dependent on the release of GH-releasing factor from the VMH-arcuate nucleus region of the brain. The data are consistent with the view that the obesity and GH suppression of the VMH syndrome reflect the disruption of two different neuronal systems.

Comments

This article was originally published in Endocrinology, 112(1): 212-219. © 1983 The Endocrine Society

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