We have developed and validated a method for measuring immunoreactive somatomedin-C (Sm-C) in serum of rabbits, and have shown that during midgestation (11–26 days; gestation = 31 days) serum Sm-C concentrations are higher in normal pregnant animals than in pregnant diabetic animals. Sm-C concentrations in the serum of 28-day gestation fetuses of diabetic rabbits (3.14 ± 0.25 U/ml) were significantly higher than in the fetuses of nondiabetic rabbits (2.31 ± 0.23 U/ml; P < 0.05). Fetuses from litters of the most severely hyperglycemie diabetic mothers (glucose > 250 mg/dl) had higher serum Sm-C (3.66 ± 0.41 U/ml) than those of mothers who were mildly hyperglycemie (2.71 ± 0.2 U/ml). Although these differences were not statistically significant, fetuses from the former litters accounted in great part for the difference between the fetuses of diabetic and normal pregnancy. The diabetes-related increment in Sm-C does not appear to be due to insulin, since fetal insulin concentrations were not different between the normal and diabetic litters (normal, 50.0 ± 3.6 μU/ml versus diabetic, 49.6 ± 7.6 μU/ml). Despite their elevation in serum Sm-C, fetuses from litters of diabetic rabbits were growth retarded in weight (26.8 ± 6.9 g and 33.8 ± 6.9 g, diabetic versus normal pregnancy; P < 0.05) and in length (7.9 ± 0.7 cm and 8.6 ± 0.7 cm, diabetic versus normal pregnancy; P < 0.025). We speculate that these discrepancies between growth and Sm-C might be secondary to the toxic effects of glucose on embryonic growth and that later in gestation, the excessive energy provided to the fetus might stimulate Sm-C synthesis.

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