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,
S. A. KAPLAN and
B. M. LIPPE
Department of Pediatrics, Division of Endocrinology and Metabolism, UCLA Center for the Health Sciences Los Angeles, California 90024
Address all correspondence and requests for reprints to: Dr. Naomi Neufeld, Department of Pediatrics-Endocrinology, Schuman Building, Room 516, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048.
Infants of diabetic mothers have hyperinsulinism at birth, presumably resulting from maternal hyperglycemia or some other derangement of maternal metabolism, and are extremely sensitive to insulin. Such infants have significantly greater numbers of insulin receptors on cord blood monocytes compared to normal infants.
To assess the role of maternal diabetic control, nine infants of insulin-dependent diabetic mothers, who were intensively treated during pregnancy, were studied. Maternal blood glucose values were measured during weekly out-patient visits throughout pregnancy, and insulin therapy was given to maintain fasting blood glucose values below 100 mg/dl. When necessary, the patie nts were hospitalized early in pregnancy in order to achieve glucose control, and all patients were hospitalized for up to 2 weeks before delivery for strict glucose control.
The mean birth weight (±SD) of these infants (3.23 ± 0.23 kg) was lower than that of nine infants of mothers with gestational diabetes not receiving insulin or intensive efforts at maintenance of normoglycemia (3.99 ± 0.12; P < 0.01) and was not significantly different from that of normal infants (3.51 ± 0.37 kg). Mean cord blood C-peptide levels (±SD), determined by RIA, were 1.6 ± 0.78 ng/ml for infants of these strictly controlled diabetic mothers and 1.4 ±0.1 ng/ml for normal infants. Scatchard analysis of [125I] insulin binding to cord blood monocytes yielded mean receptor numbers for infants of diabetic mothers of 22,500 vs. 105,000 sites/cell for infants of gestational diabetic mothers (P < 0.001) and 26,600 sites/cell for normal infants.
We conclude that the strict control of maternal diabetes during the last trimester of pregnancy prevents fetal hyperinsulinemia and is associated with the development of normal numbers of insulin receptors on the infants' monocytes.
* This work was supported in part by a grant from the KROC Foundation (to S.A.K.) and grants (to B.M.L.) from the Cystic Fibrosis Foundation and the American Diabetes Association, Inc.
Recipient of a Clinical Investigator Award from the NIAMDD (AM-K08 380).
Received October 6, 1980.
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S. A. KAPLAN, B. M. LIPPE, C. R. BRINKMAN III, M. B. DAVIDSON, and M. E. GEFFNER Diabetes Mellitus Ann Intern Med, May 1, 1982; 96(5): 635 - 649. [Abstract] [PDF] |
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