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      Control of Growth Hormone Secretion from Porcine Fetal and Neonatal Pituitary Tissue in vitro by Growth Hormone-Releasing Hormone, Somatostatin, and Insulin-Like Growth Factor

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          Abstract

          The physiological mechanism underlying the enormously elevated fetal plasma GH concentrations in mammalian species is not well understood. We postulated that a decreased sensitivity to the inhibitory effects of somatostatin (SRIH) and insulin-like growth factor-1 (IGF-1) at the pituitary level during porcine fetal life might be one factor in the high plasma GH levels. Therefore, the acute effects of GH-releasing hormone (GHRH), SRIH, and IGF-1 on GH release from the porcine anterior pituitary (AP) were studied using a perifusion system. AP tissue pieces from male and female fetuses (95 days postcoitum) and piglets (10–12 days postpartum) were perifused (at least 6 replicates per treatment and sex) at a rate of 0.1 ml/min and fractions were collected at 10-min intervals. Tissue was subjected to various treatments in random order: a 10-min GHRH pulse (1 n M) with or without concomitant 40-min exposure to SRIH (1, 10 or 100 n M) or IGF-1 (1 or 10 n M) or exposure to SRIH or IGF-1 alone (10 n M each). None of the treatments revealed sex differences, therefore data from males and females were pooled. Exposure to GHRH resulted in a rapid stimulatory GH response both in fetuses (from 61.1 ± 4.1 to 125.6 ± 4.7 ngGH· 80 mm<sup>–1</sup> · mg<sup>–1</sup> AP, p < 0.05) and neonates (from 58.1 ± 5.3to 104.6 ± 4.5 ngGH · 80 min<sup>–1</sup>·mg<sup>–1</sup> AP p < 0.05). Exposure to the lowest dose of SRIH or IGF-1 (1 n M) during GHRH pulse inhibited (p < 0.05) the GH response to GHRH in neonates (74.3 ± 3.9 and 72.5 ± 6.3 ngGH· 80 min<sup>–1</sup> · mg<sup>–1</sup> AP, respectively), but not in fetuses (115.9 ± 5.8 and 118.7 ± 5.4 ng GH-80 min<sup>–1</sup> · mg<sup>–1</sup> AP, respectively). When high doses of SRIH (10 or 100 n M) or IGF-1 (10 n M) were used, the GHRH-induced GH release was totally blocked in neonates (p < 0.05). However, in fetuses the GH response was inhibited only during the first 40 min after GHRH, and a rebound or delay effect occurred during the next 40 min. Irrespective of these general findings, some individual profiles from fetuses (4 profiles) showed that 1 n M SRIH or IGF-1 could inhibit GHRH-induced GH secretion. In contrast, individual profiles from neonates indicated that high doses of SRIH (7 profiles) or IGF-1 (5 profiles) were unable to block GH release stimulated by GHRH. On the other hand, a paradoxical stimulation of GH was observed during treatment with SRIH alone in three individual profiles from fetuses. These data confirm our hypothesis that the highly elevated plasma GH levels in the porcine fetus in vivo (compared to neonates) may be explained, at least in part, by a decreased sensitivity to the inhibitory effects of SRIH and IGF-1 at the pituitary level during fetal life. Results from some profiles indicated individual variations in the maturation of the GH control system, and moreover, even a ‘paradoxical’ enhancement of GH release in some fetal GH profiles.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1997
          1997
          09 April 2008
          : 65
          : 2
          : 117-128
          Affiliations
          aDivision of Endocrinology, Institute of Animal Husbandry and Animal Behaviour (FAL), Mariensee, Neustadt a Rbge, Germany, and bDepartment of Cell Biology, University of Cordoba, Spain
          Article
          127171 Neuroendocrinology 1997;65:117–128
          10.1159/000127171
          9067989
          © 1997 S. Karger AG, Basel

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          Page count
          Pages: 12
          Categories
          Growth Hormone

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