Serum Somatomedin-C Concentrations in a Rabbit Model of Diabetic Pregnancy

  1. Edward E Lawson
  1. Department of Pediatrics, University of North Carolina School of Medicine Chapel Hill, North Carolina
  1. Address reprint requests to A. Joseph D'Ercole, M.D., 509 Clinical Sciences Building 229H, Department of Pediatrics, University of North Carolina, School of Medicine, Chapel Hill, North Carolina 27514.

Abstract

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.

  • Received August 2, 1983.
  • Revision received October 17, 1983.
  • Accepted October 17, 1983.
No Related Web Pages
| Table of Contents