Endocrinol Metab > Volume 26(4); 2011 > Article
Endocrinology and Metabolism 2011;26(4):279-284.
DOI: https://doi.org/10.3803/EnM.2011.26.4.279    Published online December 1, 2011.
Changes in Growth Hormone-Axis Function in Nutrient Excess or Deprivation.
Seungjoon Park
Department of Pharmacology, Kyung Hee University School of Medicine, Seoul, Korea. sjpark@khu.ac.kr
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.
Key Words: Fasting, Growth hormone, Metabolism, Obesity, Somatotrope


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