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Park: Changes in Growth Hormone-Axis Function in Nutrient Excess or Deprivation
Review Article
Endocrinology and Metabolism

Endocrinology and Metabolism 2011; 26(4): 279-284.

Published online: 21 December 2011

DOI: https://doi.org/10.3803/EnM.2011.26.4.279

Changes in Growth Hormone-Axis Function in Nutrient Excess or Deprivation

Seungjoon Park

Department of Pharmacology, Kyung Hee University School of Medicine, Seoul, Korea.

Corresponding author: Seungjoon Park. Department of Pharmacology and Medical Research Center for Bioreaction to ROS and Biomedical Science Institute, Kyung Hee University School of Medicine, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Korea. Tel: +82-2-961-0913, Fax: +82-2-967-0534, sjpark@khu.ac.kr

Copyright © 2011 Korean Endocrine Society

(open-access):

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Growth hormone (GH) is produced in a select population of cells, somatotropes, located in the anterior pituitary gland. GH is released into the general circulation where it interacts with multiple peripheral tissues through its receptor, GH receptor, to regulate growth and metabolic function. GH-releasing hormone (GHRH) and somatostatin are the primary positive and negative regulators of GH secretion, respectively. More recently, ghrelin has emerged as an additional stimulatory hormone for GH release. In humans, GH levels decrease in states of nutrient excess, such as obesity, and increase in response to nutrient deprivation, such as fasting, type 1 diabetes, and anorexia nervosa. Considering that GH regulates metabolism of carbohydrate, lipid, and protein, clarifying the mechanisms by which metabolic changes alter pituitary GH synthesis and secretion will increase our knowledge on the pathophysiology and treatment of metabolic diseases. In this review, the effect of nutrient excess and nutrient deficiency on GH-axis function in humans and other mammals will be summarized, with particular emphasis on studies exploring the direct effects of systemic signals, including insulin-like growth factor 1 (IGF-1) and insulin, on somatotrope function. Additionally, new mouse models with somatotrope-specific knockout of IGF-1 and insulin receptors generated by using the Cre/loxP system will be discussed.

Keywords: Fasting, Growth hormone, Metabolism, Obesity, Somatotrope

Figures and Tables

Table 1
The impact of metabolic extremes on GH-axis function
enm-26-279-i001

GH, growth hormone; GHRH, GH-releasing hormone; GHS, growth hormone secretagogue; IGF-1, insulin-like growth factor 1.

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