Journal of the American College of Nutrition, Vol 8, Issue 3 225-234, Copyright © 1989 by American College of Nutrition

JOURNAL ARTICLE

Biphasic intrauterine growth in insulin-dependent diabetic pregnancies

T. A. Siddiqi, M. Miodovnik, F. Mimouni, E. A. Clark, J. C. Khoury and R. C. Tsang
Department of Obstetrics and Gynecology, University of Cincinnati, College of Medicine, Ohio 45267.

Early fetal growth delay (7-14 weeks of gestation) has been reported in insulin-dependent diabetic (IDD) pregnancies and in several animal models. Macrosomia is a classic feature of the infant of the IDD mother. We hypothesized therefore that a biphasic pattern of fetal growth exists in IDD pregnancies. We compared fetal growth measurements [biparietal diameter (BPD) and abdominal circumference (AC)] obtained sonographically from 106 IDD pregnancies (Class B-RT) to similar data obtained from 117 normal, nondiabetic patients. The goals for diabetic glycemic control were: fasting blood sugar less than or equal to 100 mg/dl and postprandial blood sugar less than 140 mg/dl. From one to five ultrasonographic measurements were performed at varying gestational ages in all study patients. For data analysis, one examination from each pregnancy was randomly selected by computer. Gestational age (GA) was calculated from last menstrual period and corroborated by infant physical examination (Ballard score) at birth. BPD growth pattern was biphasic in the diabetic group, described by a cubic equation: BPD = 4.99 - 0.567GA + 0.037(GA)2 - 0.0005(GA)3, R2 = 0.935. Such a biphasic pattern did not exist in the control population [BPD = -3.0323 + 0.473(gestation) - (-0.0040)(gestation)2, R2 = 0.9173]. Early growth delay was greater in fetuses that subsequently developed macrosomia (p less than 0.01). Similar results were found for AC measurements. We conclude that fetal growth delay occurs in the first half of the IDD pregnancy, followed by a phase of increased growth. The mechanism of the early growth delay is unclear. We speculate that early growth delay may be due to a "toxic" effect of glucose or other metabolite; and subsequent increased growth relates to fetal hyperinsulinism which develops from weeks 15 to 20 of gestation.

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				G. Desoye and S. Hauguel-de Mouzon The Human Placenta in Gestational Diabetes Mellitus: The insulin and cytokine network Diabetes Care, July 1, 2007; 30(Supplement_2): S120 - S126. [Full Text] [PDF]