Abstract

In protein-calorie malnutrition, serum IGF-I concentrations are low despite high GH. This GH resistance might be due to a reduced number of liver GH binding sites as suggested by studies performed in fasted rats that were refed a low protein diet. To determine whether a postreceptor defect in GH action might also contribute to the GH resistance, we measured the number and the affinity constant of the liver GH binding sites and the serum IGF-I responses to injections of recombinant bGH in hypophysectomized female rats, fed a standard (15% protein) diet (N = 25) or a low (5%) protein diet (N = 25) for 8 days. There were no significant differences in the liver GH binding capacities between the 15% and the 5% protein-fed rats, whether expressed as pmol per liver (20.6 +/- 3.5 vs 14.4 +/- 1.3; mean +/- SEM; P less than 0.2; N = 5, respectively), pmol per mg DNA (1.08 +/- 0.16 vs 0.84 +/- 0.07; P less than 0.4) or fmol per mg of protein (28.98 +/- 5.04 vs 30.26 +/- 2.00; P greater than 0.5). Likewise, the affinity constants of the GH binding sites of the 15% and the 5% protein-fed rats were not significantly different (0.78 +/- 0.05 vs 0.78 +/- 0.07 x 10(9) l/mol; P greater than 0.5). Despite these non-significant reductions in liver GH binding sites, the IGF-I responses 24 h after sc injections of increasing doses of bovine GH were blunted in the rats fed the 5% protein diet.(ABSTRACT TRUNCATED AT 250 WORDS)

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