The growth hormone (GH)-releasing hormone (GHRH)-GH-somatomedin axis

Evidence for rapid inhibition of GHRH-elicited GH release by insulin-like growth factors I and II

G. P. Ceda, R. G. Davis, Ronald (Ron) Rosenfeld, A. R. Hoffman

Research output: Contribution to journalArticle

109 Citations (Scopus)

Abstract

Hypothalamic-pituitary-end-organ axes are frequently controlled by long loop negative feedback homeostatic mechanisms. Insulin-like growth factor I (IGF-I), IGF-II, and insulin receptors have recently been described in normal and neoplastic rat and acromegalic human pituitary cells, a finding which suggests the possibility that somatomedins might exert feedback at the levels of the anterior pituitary. To study the kinetics of this feedback response, we used perifused dispersed rat anterior pituitary cells to learn if somatomedins or insulin could inhibit GH-releasing hormone (GHRH)-stimulated GH secretion. Cells were exposed to hourly boluses of 1 nM GHRH with or without varying doses of IGF or insulin. IGF-I inhibited GHRH-elicited GH release with an IC50 of 6.5 nM; maximal inhibition (~67%) was achieved with 10 nM IGF-I. IGF-II was a less potent hormone, with 10 nM inhibiting about 30% of GHRH-stimulated GH release. Slight inhibition of stimulated GH release (

Original languageEnglish (US)
Pages (from-to)1658-1662
Number of pages5
JournalEndocrinology
Volume120
Issue number4
StatePublished - 1987
Externally publishedYes

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Growth Hormone-Releasing Hormone
Insulin-Like Growth Factor II
Somatomedins
Insulin-Like Growth Factor I
Growth Hormone
Hormones
Insulin
IGF Type 2 Receptor
Insulin Receptor
Inhibitory Concentration 50

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

The growth hormone (GH)-releasing hormone (GHRH)-GH-somatomedin axis : Evidence for rapid inhibition of GHRH-elicited GH release by insulin-like growth factors I and II. / Ceda, G. P.; Davis, R. G.; Rosenfeld, Ronald (Ron); Hoffman, A. R.

In: Endocrinology, Vol. 120, No. 4, 1987, p. 1658-1662.

Research output: Contribution to journalArticle

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