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Endocrinology, Vol 117, 1132-1138, Copyright © 1985 by Endocrine Society

ARTICLES

Effects of intracellular glucopenia on pulsatile growth hormone secretion: mediation in part by somatostatin

JC Painson and GS Tannenbaum

We examined the effects of 2-deoxy-D-glucose (2DG)-induced intracellular glucoprivation on GH, insulin, and glucose secretory dynamics in freely moving rats bearing chronic intracerebroventricular and intracardiac venous cannulae. Intravenous administration of 2DG (400 mg/kg) caused a severe suppression in amplitude and duration of spontaneous GH surges; plasma GH levels remained significantly depressed for at least 5 h in the presence of marked hyperglycemia. Plasma insulin levels were unchanged. Central administration of a low dose of 2DG (8 mg/10 microliters) also markedly attenuated GH pulse amplitude and raised plasma glucose levels, but this low dose was without effect when injected peripherally, suggesting a central site of action. To elucidate the mechanism(s) mediating the GH suppression response to insufficient glucose we assessed the involvement of the two hypothalamic GH-regulatory peptides, somatostatin (SRIF) and GH- releasing factor (GRF). Passive immunization of 2DG-treated rats with a specific SRIF antiserum (AS) caused an initial surge of GH release and significant elevation of both trough and mean 6-h plasma GH levels, compared to 2DG-normal sheep serum controls. However, SRIF AS failed to restore the amplitude of GH pulses to normal levels. Administration of three iv boluses of human GRF (10 micrograms), at 90-min intervals, to 2DG-treated rats resulted in GH release which was variable and time dependent; the magnitude of the first response (1 h after 2DG injection) was significantly less than that of the other two. Immunoneutralization with SRIF AS eliminated this difference and significantly enhanced human GRF-induced GH release. These results demonstrate that intracellular glucopenia is a potent inhibitor of pulsatile GH secretion in the rat and that this response is mediated, in part, by an increase in SRIF release. While the present findings are compatible with the hypothesis that glucoprivation induces an acute SRIF release, only a partial role for SRIF is indicated in this response. The longer lasting suppression of GH pulses observed after glucose deprivation may be due to decreased output of GRF from the hypothalamus.




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Copyright © 1985 by The Endocrine Society