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Journal of Clinical Endocrinology & Metabolism Vol. 63, No. 6 1300-1306
doi:10.1210/jcem-63-6-1300
Copyright © 1986 by the Endocrine Society.
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Serum Levels of Somatomedins and Somatomedin-Binding Protein in Pregnant Women with Type I or Gestational Diabetes and Their Infants*

KERSTIN HALL, ULF HANSSON, GUNNEL LUNDIN, MARGUERITE LUTHMAN, BENGT PERSSON, GUILHERME PÓVOA{dagger}, MAGNUS STANGENBERG and ULRIKA ÖFVERHOLM

Departments of Endocrinology and Obstetrics and Gynecobgy, Karolinska Hospital, and the Department of Pediatrics, St Göran's Children's Hospital Stockholm, Sweden

Address requests for reprints to: Dr. Kerstin Hall, Department of Endocrinology, Karolinska Institutet, Box 60500, Stockholm, S-10401, Sweden.

The serum levels of the low mol wt form of somatomedin-binding protein (SMBP) were 5-fold higher in both diabetic (n = 44) and nondiabetic pregnant women (n = 14) than in nonpregnant women. No difference was found between women with type 1 diabetes and those with gestational diabetes.

There was a negative correlation between maternal levels of SMBP during the last trimester and the birth weight percentile of the infants (r = –0.51). There was a 2- to 3-fold elevation of maternal insulin-like growth factor (IGF-I) levels during pregnancy in both diabetic and nondiabetic women. A positive correlation (r = 0.49) was found between maternal IGF-I levels and the birth weight percentiles of their infants. The correlation between the ratio of IGF-I to SMBP, which may reflect the IGFI available to the placenta, to birth weight percentile was higher (r = 0.57), and the SE of estimate of weight percentile was 23%. The ratio between IGF-I and SMBP in cord blood was correlated with birth weight, although cord blood IGF-I and SMBP values were not. The IGF-II levels in cord serum were 50% higher in the infants of diabetic than in those of nondiabetic mothers.

These findings raise the questions of whether maternal SMBP levels influence the amount of IGF-I available for the fetal-placental unit and whether IGF-II participates in glucose homeostasis in the fetus.

* This work was supported by grants from the Swedish Medical Research Council (no. 4224 and 3787).

{dagger} Recipient of a scholarship from CAPES/Education and Culture Ministry, Brazil.

Received January 16, 1986.




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