RESUMO
Rat hypothalamic somatostatin (SRIF) release in vitro is inversely related to medium glucose concentration and is stimulated by agents interfering with neural glucose uptake or metabolism. The present studies examined monosaccharide specificity of this effect by comparing the ability of glucose and nonmetabolized sugars (ribose, fructose, and galactose) to reverse glucopenia-mediated SRIF release. Removal of glucose from incubation medium resulted in a 7-fold stimulation of hypothalamic SRIF release (24.9 +/- 3.0 to 169.0 +/- 46.2 pg/5 min) that was promptly and fully reversed by readdition of glucose (21.5 +/- 6.0 pg/5 min). Depolarizing concentrations of potassium (40 mM) added to medium after incubation in the presence or absence of glucose produced similar 4-fold biphasic stimulation of SRIF release, suggesting that tissue viability was unimpaired by short term glucopenia. By contrast, nonmetabolized sugars (ribose, fructose, or galactose) at concentrations up to 28 mM were unable to reverse glucopenia-mediated hypothalamic SRIF release. These findings suggest that neural metabolism of glucose specifically influences hypothalamic SRIF release, an effect likely to depend on glycolysis with resulting energy production. This explanation is supported by the finding that the glycolytic intermediates dihydroxyacetone and glyceraldehyde were partly, and pyruvate completely, able to restore glucopenia-mediated SRIF release toward basal, with a maximal effect at 14 mM. Our present studies suggest that rat hypothalamic SRIF release reflects ambient glucose status, is stimulated by glucopenia, and may explain inhibition of GH secretion in the rat during hypoglycemia.
