DECREASED SERUM SOMATOMEDIN-C (Sm-C) RESPONSE TO GROWTH HORMONE (GH) IN HYPOPHYSECTOMIZED RATS FED A LOW PROTEIN DIET: EVIDENCE FOR A POSTRECEPTOR DEFECT

Abstract

Reduced number of liver GH receptors may participate to the fall of Sm-C in fasted and protein restricted rats. However, a possible role for a postreceptor defect has not been evaluated. To address this question, the liver GH binding sites and the serum Sm-C responses to single injections of saline or bovine GH (0.25; 0.5; 1 and 5 mg/rat; 5 rats/dose) were determined in hypophysectomized female rats, submitted for 7 days to a normal (15 %; n = 25) or a low protein diet (5 %; n = 25). Binding studies were performed with 125I-bovine GH. The liver GH binding capacities (pmol/mg DNA; mean ± SE) of the low protein-fed rats (0.85 ± 0.07) were not significantly different (P > 0.05) from those of normal protein-fed animals (1.09 ± 0.16). Also, the affinity constants were not affected by protein intake. Basal serum Sm-C levels, determined by RIA, were similar in both groups and increased in a dose-dependent manner in response to GH. However for each GH dose, the Sm-C response in the low protein-fed rats was lower. The maximal Sm-C response to GH (5 mg) was in the malnourished rats (0.13 ± 0.04 U/ml) significantly reduced when compared to the controls (0.36 ± 0.03 U/ml; P< 0.001).In conclusion, the blunted maximal Sm-C response to GH together with unaltered liver GH binding suggest that protein malnutrition induces a GH postreceptor defect.