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Endocrine Control of Growth



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    • Philip Murray graduated in Medicine from Glasgow University and trained in pediatrics in Manchester, Melbourne, and London. He now works as National Institute Health Research (NIHR) Clinical Lecturer in pediatric endocrinology at the University of Manchester and Royal Manchester Children' Hospital.

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    • Correspondence to: Professor Peter Clayton, 5th Floor (Research), Royal Manchester Children's Hospital Oxford Road, Manchester, M13 9WL, UK. E-mail:

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    • Peter Clayton is Professor of Child Health and Paediatric Endocrinology at the University of Manchester and an honorary consultant at the Royal Manchester Children's Hospital with a particular interest in the disorders and physiology of growth. His clinical and research interests include the mechanisms of normal and disordered growth.

  • The authors declared that they have no conflicts of interest.
  • Correction added on 12th July 2017, after initial online publication. A duplicate of this article was published under the DOI 10:1002/j.1552-4876.2013.31357.x. This duplicate has now been deleted and its DOI redirected to this version of the article.


Human growth is a complex process starting at conception and completing in adolescence at the time of growth plate fusion. Growth can be divided into four phases: (1) fetal, where the predominant endocrine factors controlling growth are insulin and the insulin-like growth factors. (2) Infancy, where growth is mainly dependent upon nutrition. (3) Childhood, where the growth hormone–insulin-like growth factor-I (GH-IGF-I) axis and thyroid hormone are most important. (4) Puberty, where along with the GH-IGF-I axis the activation of the hypothalamo-pituitary–gonadal axis to generate sex steroid secretion becomes vital to the completion of growth. GH is released from the pituitary in a pulsatile fashion under the control of GHRH, Ghrelin, and somatostatin and, via a complex signal transduction cascade, initiates the release of IGF-I within many tissues but predominantly the liver and at the growth plate. IGF-I acts in an autocrine and paracrine manner via the IGF-I receptor to stimulate cell proliferation and longitudinal growth. Activation of the pituitary–gonadal axis during puberty occurs via a complex interaction of factors including kisspeptin, leptin, gonadotrophin releasing hormone, and tachykinin ultimately leading to augmentation of GH secretion, the pubertal growth spurt, and fusion of the growth plates. Many other hormones can affect the GH-IGF-I system or directly affect cell proliferation at the growth plate including thyroid hormone, vitamin D, and corticosteroids. © 2013 Wiley Periodicals, Inc.