Recent studies have suggested a partial block in somatomedin (SM) production or growth hormone (GH) action in IDDM. Twelve well-nourished diabetic children (9 males and 3 females with a mean age of 11.2 ± 3.3 yr), six with an HbA1c of 7.9–11.2% (group A) and six with an HbA1c of 12.5–15.6% (group B), were studied as follows: the GH response after 100 μg of oral clonidine and the SM generation capacity after i.m. administration of 0.2 U/kg/dose of human growth hormone (hGH) for 4 days. Group B diabetic subjects had a significantly higher mean ± SD GH increase after clonidine than did group A patients (Δ of 17.4 ± 4.9 versus 5.7 ± 6.0 ng/ml, P < 0.01); the basal GH of both groups were similar (1.6 ± 0.7 versus 2.3 ± 1.4 ng/ml). In contrast, the SM response to hGH was significantly decreased in group B children as compared with those in group A (Δ of 0.3 ± 0.3 versus 1.2 ± 0.4 U/ml, P ± 0.01). The basal SM levels of both groups were normal for age. GH and SM correlated with HbA1c levels (r = +O.80, P < 0.01; r = −0.79, P < 0.01, respectively); there was no correlation with plasma and urine glucose or serum cholesterol, cortisol, and transferrin. Our data indicate a blunted SM response to hGH in group B diabetic subjects; this defect in SM generation is apparently not present in group A subjects. A biologically inactive GH molecule and poor nutrition seem unlikely, but circulating inhibitory factors not picked up by our radioimmunoassay, the degree of diabetes control, or a still unclear metabolic derangement may be contributing to this defect.

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