Long-Term Inhibitory Effects of Somatostatin and Insulin-Like Growth Factor 1 on Growth Hormone Release by Serum-Free Primary Culture of Pituitary Cells from European Eel (Anguilla anguilla).

Autor: Rousseau, Karine, Yung-Sen Huang, Karine, Le Belle, Nadine, Vidal, Bernadette, Marchelidon, Jacques, Epelbaum, Jacques, Dufour, Sylvie
Předmět:
Zdroj: Neuroendocrinology; 1998, Vol. 67 Issue 5, p301-309, 9p, 1 Black and White Photograph, 1 Chart, 3 Graphs
Abstrakt: To investigate the ability of hypothalamic and peripheral factors to directly regulate growth hormone (GH) release in a primitive teleost, the European eel (Anguilla anguilla L.), we used primary cultures of dispersed pituitary cells. When cultured for 12 days in a serum-free medium, pituitary cells continuously released large amounts of GH, which exceeded the initial cellular content. Somatotropin-release inhibiting hormone (SRIH-14) dose-dependently inhibited GH release (EC[sub 50] 0.75 nM) up to a maximal inhibitory effect of 95%. No desensitization of somatotropes to SRIH was observed over the 12 days of culture. Use of receptor subtype-selective SRIH agonists suggests the existence on eel somatotropes of SRIH receptor(s) related to the mammalian sst[sub 2] /sst[sub 3] /sst[sub 5] class rather than to the sst[sub 1] /sst[sub 4] class. Insulin-like growth factor 1 (IGF1) dose-dependently inhibited GH release (EC[sub 50] 0.03 nM) up to a maximal inhibitory effect of 85%, without desensitization. IGF1 and IGF2 were equipotent in inhibiting GH release, whereas insulin was 1,000 times less active, suggesting the implication of a receptor related to the mammalian IGF type 1 receptor. These results indicate that eel somatotropes are active in vitro without any specific additional factors, and suggest the existence of a dominant inhibitory control of GH release in vivo. Two potential candidates for this chronic negative regulation are a neurohormone, SRIH and a circulating factor, IGF1. These data underline the early evolutionary origin of the molecular and functional SRIH-GH-IGF1 neuroendocrine axis in vertebrates. [ABSTRACT FROM AUTHOR]
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