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 < 0.2; N = 5, respectively), pmol per mg DNA (1.08 ± 0.16 vs 0.84 ± 0.07; P <0.4) or fmol per mg of protein (28.98 ± 5.04 vs 30.26 ± 2.00; P > 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 × 109 l/mol; P > 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. The maximal IGF-I response in the rats with the normal protein intake was 360 ± 30 U/I, but only 130 ± 40 U/l in the 5% protein-fed animals (P < 0.001). The blunted serum IGF-I responses to GH, together with decreased maximal stimulation in the 5% protein-fed hypophysectomized rats, support the possibility that a postreceptor defect in GH action contributes to the GH resistance in protein-calorie malnutrition.