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Effects of Glucose on Thyrotrophin‐Releasing Hormone, Growth Hormone‐Releasing Hormone, Somatostatin and Luteinizing Hormone‐Releasing Hormone Release from Rat Hypothalamus in vitro
Author(s) -
Lewis B. M.,
Dieguez C.,
Ham J.,
Page M. D.,
Creagh F. M.,
Peters J. R.,
Scanlon M. F.
Publication year - 1989
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.1989.tb00144.x
Subject(s) - somatostatin , medicine , endocrinology , growth hormone–releasing hormone , hypothalamus , hormone , luteinizing hormone , chemistry , gonadotropic cell , somatotropic cell , thyrotropin releasing hormone receptor , neuropeptide , peptide hormone , in vitro , biology , hormone receptor , growth hormone , receptor , biochemistry , cancer , breast cancer
Increasing concentrations of D‐glucose (1 to 25 mM) inhibited somatostatin, thyrotrophin‐releasing hormone (TRH) and growth hormone‐releasing hormone (GHRH) release from incubated adult rat hypothalami in a stereospecific manner. In contrast, the effects of D‐ and L‐glucose on luteinizing hormone‐releasing hormone release were virtually identical. Increasing concentrations of D‐glucose also inhibited somatostatin release following depolarization with high K + , but had no obvious effect on depolarization‐induced TRH or GHRH release when compared with L‐glucose. In conclusion, D‐glucose exerts a potent, dose‐related modulatory action on the release of rat hypothalamic TRH and GHRH as well as somatostatin in vitro. Further studies are required to establish any physiological relevance of glucose in the modulation of these hypothalamic neuropeptides.