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      Differential Sensitivity of Growth Hormone-Releasing Hormone and Somatostatin Release from Perifused Mouse Hypothalamic Fragments in Response to Glucose Deficiency

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          Abstract

          The effects of glucose deficiency on growth hormone (GH)-releasing hormone (GRH) and somatostatin (SRIH) release from mouse hypothalamic fragments were investigated using an in vitro perifusion system. Fragments were perifused with Krebs-Ringer bicarbonate solution (KRB) containing 5.6 m M glucose for 3 h followed by reduced glucose concentrations in KRB for the next 2 h. GRH release was simulated by 0.7-2.8 m M glucose in an inverse concentration-dependent manner. In contrast, SRIH release was not stimulated by glucose at concentrations of 2.8 and 1.4 m M; only at 0.7 m M was there a modest stimulation of SRIH release that was comparable to the effect of 2.8 m M glucose on GRH release. The maximal stimulation of GRH and SRIH release by 0.7 m M glucose was 221 and 150%, respectively, of controls. Glucose concentrations of 11.2 and 22.4 m M inhibited GRH release but did not alter SRIH release. The glucose analog 2-deoxy-D-glucose (2-DG; 5.6-39.2 m M) also stimulated GRH release in a dose-dependent manner, and SRIH release was less sensitive to 2-DG than was GRH. The maximal stimulation of GRH and SRIH release by 39.2 mM2-DG was 190 and 147%, respectively, of controls. Increases in GRH and SRIH release stimulated by 30 m M KC1 1 h after exposure to low glucose or 2-DG were not significantly different from those after exposure to 5.6 m M glucose. However, the SRIH response to K<sup>+</sup>-induced depolarization was much greater than that of GRH. The glucose intermediate pyruvate (4.9 and 9.8 m M) partially inhibited both GRH and SRIH release induced by 0.7 m M glucose. The glutamate receptor antagonist 2-amino-7-phosphonoheptanoic acid also partially inhibited the GRH release induced by 0.7 m M glucose. These results indicate that mouse hypothlaamic GRH release is more sensitive to the inhibition of intracellular glycolysis than is SRIH release. Although inhibition of glycolysis appears to mediate glucopenia-induced GRH and SRIH release, the predominance of GRH release cannot be explained by nonspecific membrane depolarization subsequent to energy reduction. An additional mechanism involved in the specific release of GRH induced by glucose deficiency may relate to activation of endogenous glutamate receptor activity.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1993
          1993
          08 April 2008
          : 57
          : 6
          : 1097-1105
          Affiliations
          Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
          Article
          126476 Neuroendocrinology 1993;57:1097–1105
          10.1159/000126476
          7901785
          © 1992 S. Karger AG, Basel

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          Page count
          Pages: 9
          Categories
          Original Paper

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