INTERACTIONS BETWEEN GROWTH-HORMONE AND NUTRITION IN HYPOPHYSECTOMIZED RATS - BODY-COMPOSITION AND PRODUCTION OF INSULIN-LIKE GROWTH FACTOR-I

Hypophysectomy of adult rats results in a loss of body growth which ca n be reversed by treatment with GH. The increased growth caused by adm inistration of GH is accompanied by an increase in food consumption. T he effects of GH and interactions with nutrition were investigated by treating hypophysectomized rats with GH and either providing unrestric ted food or preventing the increased food consumption by pair-feeding with the same intake as that of the hypophysectomized animals. Over th e 7-day experimental period, the GH-treated animals grew significantly when food was available ad libitum but did not gain body weight when an increase in food intake was prevented. However, there was a signifi cant interaction between GH and nutrition on body composition; GH sign ificantly decreased body fat and increased the protein: fat ratio only in the animals with the restricted intake. Gastrocnemius muscle weigh t was increased by GH regardless of food intake, but heart weight did not increase and liver weight was actually decreased by GH treatment w hen food intake was restricted. Serum concentrations of insulin and in sulin-like growth factor-I (ICF-I) were increased by GH in the rats wi th food available ad libitum but not in the pair-fed rats. However, th e liver concentration of IGF-I and its mRNA were increased by GH altho ugh the increase in IGF-I mRNA was modulated by the restricted food in take. The decreased weight of the liver in the pair-fed GK-treated rat s, despite the increase in IGF-I mRNA, suggests that IGF-I does not in fluence liver growth. In the gastrocnemius muscle, however, GH increas ed IGF-I mRNA concentration similarly in both rats with food available ad libitum and in pair-fed rats. Decreased nutrition therefore modula ted the action of GH but emphasized its nutrient partitioning effect, thus increasing the anabolic drive towards skeletal-muscle growth; thi s appeared to be mediated by the local production of IGF-I within the muscle.