Hyperinsulinemia in Cord Blood in Mothers With Type 2 Diabetes and Gestational Diabetes Mellitus in New Zealand
- Jenny A. Westgate, FRANZCOG, MD,
- Robert S. Lindsay, MB, PHD2,
- Judith Beattie, RM3,
- Neil S. Pattison, FRANZCOG, MD3,
- Greg Gamble, MSC4,
- Lindsay F.J. Mildenhall, FRACP5,
- Bernhard H. Breier, PHD6 and
- Frank D. Johnstone, FRCOG, MD7
- 1Department of Obstetrics and Gynecology, University of Auckland, Auckland, New Zealand
- 2Western Infirmary, British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, U.K.
- 3Department of Women’s Health, Middlemore Hospital, Auckland, New Zealand
- 4Clinical Trials Research Unit, Faculty of Medicine and Health Sciences, University of Auckland, Auckland, New Zealand
- 5Department of Newborn Services, Kid First, Middlemore Hospital, Auckland, New Zealand
- 6Liggins Institute, University of Auckland and Research Centre for Growth and Development, Auckland, New Zealand
- 7Obstetrics Department, University of Edinburgh, Edinburgh, Scotland, U.K.
- Address correspondence and reprint requests to Dr. Jenny Westgate, Obstetrics and Gynecology, University of Auckland, Private Bag, 92019 Auckland, New Zealand. E-mail: ja.westgate{at}auckland.ac.nz
Abstract
OBJECTIVE—In genetically diabetes-prone populations, maternal diabetes during pregnancy increases the risk of their children developing diabetes and obesity (the vicious cycle of type 2 diabetes). Fetal hyperinsulinemia at birth acts as a marker of this risk. We therefore examined whether cord insulin and leptin concentrations are increased in offspring of Maori and Pacific Island mothers with type 2 and gestational diabetes mellitus (GDM) and varying degrees of glycemic control (HbA1c).
RESEARCH DESIGNS AND METHODS—Maori and Pacific Island mothers were prospectively recruited at Middlemore Hospital, South Auckland. Cord blood was taken from umbilical vein at birth from singleton babies born after 32 weeks of gestation to 138 mothers with GDM, 39 mothers with type 2 diabetes, and 95 control mothers.
RESULTS—Babies born to mothers with both type 2 diabetes and GDM had higher birth weight and skinfold thickness and markedly higher concentrations of insulin (median [interquartile range] type 2 diabetes 77 pmol/l [42–143], GDM 67 pmol/l [42–235], and control subjects 33 pmol/l [18–62]; P < 0.001) and leptin (type 2 diabetes 39 ng/ml [18–75], GDM 31 ng/ml [17–58], and control subjects 13 ng/ml [8–22]; P < 0.001) in cord blood. Cord insulin concentrations >120 pmol/l were found in 29% of offspring of mothers with GDM and 31% of mothers with type 2 diabetes. Many mothers with GDM had abnormalities of glucose tolerance postpartum (20% type 2 diabetes, 34% impaired glucose tolerance or impaired fasting glucose). Higher cord insulin (57 pmol/l [40–94]) and leptin (26 ng/ml [17–39]) concentrations were found even in offspring of GDM mothers with normal glucose tolerance postpartum.
CONCLUSIONS—Raised cord insulin and leptin concentrations are a common finding in offspring of mothers with type 2 diabetes and GDM in this population.
Footnotes
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A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.
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- Accepted February 26, 2006.
- Received September 8, 2005.
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