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      Is Open Access

      Growth Hormone and Reproduction: A Review of Endocrine and Autocrine/Paracrine Interactions

      review-article
      Author(s): 1 , 2 , * , 3
      Publication date (Electronic):
      Journal: International Journal of Endocrinology
      Publisher: Hindawi Publishing Corporation

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          Abstract

          The somatotropic axis, consisting of growth hormone (GH), hepatic insulin-like growth factor I (IGF-I), and assorted releasing factors, regulates growth and body composition. Axiomatically, since optimal body composition enhances reproductive function, general somatic actions of GH modulate reproductive function. A growing body of evidence supports the hypothesis that GH also modulates reproduction directly, exerting both gonadotropin-dependent and gonadotropin-independent actions in both males and females. Moreover, recent studies indicate GH produced within reproductive tissues differs from pituitary GH in terms of secretion and action. Accordingly, GH is increasingly used as a fertility adjunct in males and females, both humans and nonhumans. This review reconsiders reproductive actions of GH in vertebrates in respect to these new conceptual developments.

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          Most cited references347

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          Insulin-like growth factors and their binding proteins: biological actions.

          D Clemmons, J Jones (1995)
          Article 0 comments Cited 357 times – based on 0 reviews     Review now
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            Medical progress: Acromegaly.

            Shlomo Melmed (2006)
            Article 0 comments Cited 277 times – based on 0 reviews     Review now
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              Effects of growth hormone on glucose, lipid, and protein metabolism in human subjects.

              Niels Frimodt Møller, Jens Otto Lunde Jørgensen (2009)
              In evolutionary terms, GH and intracellular STAT 5 signaling is a very old regulatory system. Whereas insulin dominates periprandially, GH may be viewed as the primary anabolic hormone during stress and fasting. GH exerts anabolic effects directly and through stimulation of IGF-I, insulin, and free fatty acids (FFA). When subjects are well nourished, the GH-induced stimulation of IGF-I and insulin is important for anabolic storage and growth of lean body mass (LBM), adipose tissue, and glycogen reserves. During fasting and other catabolic states, GH predominantly stimulates the release and oxidation of FFA, which leads to decreased glucose and protein oxidation and preservation of LBM and glycogen stores. The most prominent metabolic effect of GH is a marked increase in lipolysis and FFA levels. In the basal state, the effects of GH on protein metabolism are modest and include increased protein synthesis and decreased breakdown at the whole body level and in muscle together with decreased amino acid degradation/oxidation and decreased hepatic urea formation. During fasting and stress, the effects of GH on protein metabolism become more pronounced; lack of GH during fasting increases protein loss and urea production rates by approximately 50%, with a similar increase in muscle protein breakdown. GH is a counterregulatory hormone that antagonizes the hepatic and peripheral effects of insulin on glucose metabolism via mechanisms involving the concomitant increase in FFA flux and uptake. This ability of GH to induce insulin resistance is significant for the defense against hypoglycemia, for the development of "stress" diabetes during fasting and inflammatory illness, and perhaps for the "Dawn" phenomenon (the increase in insulin requirements in the early morning hours). Adult patients with GH deficiency are insulin resistant-probably related to increased adiposity, reduced LBM, and impaired physical performance-which temporarily worsens when GH treatment is initiated. Conversely, despite increased LBM and decreased fat mass, patients with acromegaly are consistently insulin resistant and become more sensitive after appropriate treatment.
              Article 0 comments Cited 259 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Endocrinol
                Journal ID (iso-abbrev): Int J Endocrinol
                Journal ID (publisher-id): IJE
                Title: International Journal of Endocrinology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1687-8337
                ISSN (Electronic): 1687-8345
                Publication date (Print): 2014
                Publication date (Electronic): 15 December 2014
                Volume: 2014
                Electronic Location Identifier: 234014
                Affiliations
                1Department of Biology, Bishop's University, Sherbrooke, QC, Canada J1M 1Z7
                2Centre de Recherche Clinique Etienne-Le Bel, Université de Sherbrooke, Sherbrooke, QC, Canada J1H 5N4
                3Department of Physiology, University of Alberta, Edmonton, AB, Canada T6G 2R3
                Author notes

                Academic Editor: Maria L. Dufau

                Article
                DOI: 10.1155/2014/234014
                PMC ID: 4279787
                PubMed ID: 25580121
                SO-VID: 6f41a471-1cfd-46c3-a5d1-0ac1630f09cd
                Copyright © Copyright © 2014 K. L. Hull and S. Harvey.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 23 October 2014
                Date accepted : 26 November 2014
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Endocrinology & Diabetes
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes

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