Low circulating somatomedin-C/insulin-like growth factor I in insulin-dependent diabetes and malnutrition: growth hormone receptor and post-receptor defects.

Abstract

Although growth hormone (GH) is the principal stimulus for somatomedin (SM) production (Van Wyk, 1984), serum SM concentrations are reduced markedly despite normal or elevated GH in children with poorly controlled insulin-dependent diabetes or protein-calorie malnutrition (Winter et al., 1980; Grant et al., 1973). Furthermore, rats that are diabetic or chronically protein-deficient have low serum SM concentrations that do not increase after injection of GH (Phillips and Young, 1976; Shapiro and Pimstone, 1978). The in vitro production of SM by the livers of such diabetic or protein-deprived animals is reduced, and cannot be restored to normal by GH added in vitro (Miller et al., 1981; Shapiro et al., 1978). These observations suggest that the liver in insulin-dependent diabetes and in malnutrition is resistant to GH action. This paper reviews studies directed at determining the mechanisms responsible for this hepatic GH resistance. Specifically, we have sought to determine whether the GH resistance present in diabetes and malnutrition is due to alterations of GH receptors or to post-receptor defects.