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Comparison of the effects of growth hormone

Comparison of the effects of growth hormone and insulin-like growth factor I on substrate oxidation and on insulin sensitivity in growth hormone-deficient humans.


HGH therapy reduce Insulin sensitivity, IGF-1 enhance insulin sensitivity, both medications promote protein anabolism, lipolysis and lipid oxidation and reduce protein oxidation by different mechanism. The study suggests that combined use of IGF-1 and HGH has great potential and synergistic effect.

Insulin-like growth factor-I ( IGF-I) is considered to be the mediator of the growth-promoting effects of growth hormone ( GH). The metabolic effects of these two hormones, however, are different. Whereas GH treatment leads to elevated insulin and glucose levels, reduced insulin sensitivity, and impaired glucose tolerance, IGF-1 treatment leads to reduced insulin and GH levels and enhanced Insulin sensitivity. IGF-I may, therefore, not only be the mediator of the growth-promoting effects of GH but also a modulator of the effects of GH on insulin action and glucose metabolism. To study the influence of GH and IGF-I on substrate metabolism and insulin sensitivity (assessed by euglycemic, hyper-insulinemic clamping combined with indirect calorimetry and glucose tracer infusion), we have treat. eight GH-deficient adults with GH (2 IU/m. daily subcutaneously fs.c.)), 1GF-1 (10 mcg/kg • h s.c.), or both hormones together for 7 d, respectively, and compared the effects of these treatment regimens with a control phase. Our findings suggest that (a) both GH and IGF-I promote lipolysis and lipid oxidation, albeit by different mechanisms; (b ) treatment with either hormone is followed by enhanced energy expenditure and reduced protein oxidation; and (e) IGF-I reverses the insulin resistance induced by GH. (J. Clin. Invest. 1994.94:1126-1133.)

Effects of GH and IGF-1 on protein oxidation.

Reduction of protein oxidation, i.e., of proteolysis, was observed under IGF-I as well as GH treatment. When both hormones were given together, the effects of IGF-I and GH were additive. These findimgs support those of a previous report also showing that anabolism may be stimulated to a greater extent by treatment with GH and IGF-I together than by either hormone alone (40). Moreover, insulin-like properties of IGF-I 30) and the fact that IGF-I increases insulin sensitivity of skeletal muscle may allow us to preserve normal glucose tolerance when GH and IGF-I stimulate protein anabolism in a concerted fashion.

In conclusion, our results show that IGF-I per se is a potent anticatabolic agent (as in regard to protein metabolism) leading by way of partial inhibition of insulin secretion to increased lipolysis and fat oxidation. These effects of IGF-I are indepenedent of the inhibitory effect on growth hormone secretion. All these effects of IGF-1 are, however, synergistic to those of GH, which stimulates lipolysis and possibly protein anabolism through mechanisms different from those of IGF-1. In the case of simultaneous administration of GH and IGF-1, insulin levels lie between those attained by IGF-I treatment alone and those observed during GH treatment. Since insulin is an important anabolic hormone (41), it is conceivable that in situations of severe catabolism a combination of GH and IGF-I together will turn out to give the best results with regard to anticatabolism and anabolism (40).


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