Biological effects of growth hormone on carbohydrate and lipid metabolism

Abstract This review will summarize the metabolic effects of growth hormone (GH) on the adipose tissue, liver, and skeletal muscle with focus on lipid and carbohydrate metabolism. The metabolic effects of GH predominantly involve the stimulation of lipolysis in the adipose tissue resulting in an inc...

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Bibliographic Details
Published in:Growth hormone & IGF research 2010-02, Vol.20 (1), p.1-7
Main Authors: Vijayakumar, Archana, Novosyadlyy, Ruslan, Wu, YingJie, Yakar, Shoshana, LeRoith, Derek
Format: Article
Language:English
Subjects:
Adipose Tissue - metabolism
Advanced Basic Science
Animals
Carbohydrate
Carbohydrate Metabolism - physiology
Endocrinology & Metabolism
Female
Growth Hormone - physiology
Humans
Insulin resistance
Insulin Resistance - physiology
Insulin-Like Growth Factor I - metabolism
Lipid Metabolism - physiology
Lipids
Liver - metabolism
Male
Metabolism
Mice
Muscle, Skeletal - metabolism
Proteins - metabolism
Rats
Signal Transduction - physiology
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Summary:Abstract This review will summarize the metabolic effects of growth hormone (GH) on the adipose tissue, liver, and skeletal muscle with focus on lipid and carbohydrate metabolism. The metabolic effects of GH predominantly involve the stimulation of lipolysis in the adipose tissue resulting in an increased flux of free fatty acids (FFAs) into the circulation. In the muscle and liver, GH stimulates triglyceride (TG) uptake, by enhancing lipoprotein lipase (LPL) expression, and its subsequent storage. The effects of GH on carbohydrate metabolism are more complicated and may be mediated indirectly via the antagonism of insulin action. Furthermore, GH has a net anabolic effect on protein metabolism although the molecular mechanisms of its actions are not completely understood. The major questions that still remain to be answered are (i) What are the molecular mechanisms by which GH regulates substrate metabolism? (ii) Does GH affect substrate metabolism directly or indirectly via IGF-1 or antagonism of insulin action?
ISSN:1096-6374
1532-2238
DOI:10.1016/j.ghir.2009.09.002