Growth hormone (GH), the main regulator for post-natal growth, has important metabolic actions on different tissues, similar or opposite to insulin like growth factor I (IGF-I), mainly produced by the liver after the binding of GH to its receptor. Experiments with animal models indicate an important role of GH on insulin resistance although the IGF-I role is not yet completely established. In humans, GH promotes an increase on lypolisis and lipid oxidation, while IGF-I leads to an increase on lipid oxidation only in a chronic way. While growth actions are time-limited, metabolic and cardiovascular actions of the GH/IGF-I axis are throughout life. GH anabolic effects have been used on chronic and hypercatabolic conditions, although investigations on the clinical outcomes are still scarce. In this paper, we intend to review GH metabolic actions experienced by animal models, studies with normal humans and GH deficient individuals, individuals with diabetes mellitus type 1 and metabolic syndrome individuals, hypercatabolic states and the relationship between GH and adipokines, endothelial disfunction and atherogenesis
Lypolisis; ghrelin; insulin-like growth factor I; metabolism; insulin resistance
