Growth promoting activity of IGF-I in the rat.

Abstract

According to the original somatomedin hypothesis, GH promotes growth by generating 'somatomedins' or insulin-like growth factors (IGFs) in the liver. The advent of large amounts of IGF-I produced by recombinant DNA technology has now allowed testing of this hypothesis, by comparing the growth promoting activity of IGF-I and GH in three animal models of growth deficiency. When injected or infused subcutaneously, or infused intravenously, IGF-I is a weak growth promoter in the hypophysectomized rat compared with GH, even when infused in combination with small amounts of GH. Growth arrest in the diabetic rat was corrected by insulin infusion which also restored GH secretion. Insulin or IGF-I caused a large initial weight gain in diabetic rats, accompanied by a partial correction of food and water balance, even in the presence of persistent hyperglycaemia. A new mutant GH deficient dwarf rat grows in response to both GH and IGF-I infusions, but these agents elicit different patterns of organ growth. For the same overall body growth, GH was more effective in stimulating bone growth, whereas IGF-I stimulated renal and splenic growth. This new dwarf rat may prove useful for the study of the relative growth promoting effects of IGF-I and GH in more detail in future.