Adult obesity and growth in childhoodBMJ 2002; 324 doi: https://doi.org/10.1136/bmj.324.7338.674/a (Published 16 March 2002) Cite this as: BMJ 2002;324:674
Fuel mediated teratogenesis driven by maternal obesity may be responsible for pandemic of obesity
- David Simmons ([email protected]), foundation chair in rural health,
- Bernhard H Breier, associate professor
- Department of Rural Health, University of Melbourne, PO Box 6500, Shepparton, Victoria 3630, Australia
- Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Grafton, Auckland, New Zealand
- Section of Reproductive and Developmental Medicine, University of Sheffield, Sheffield S10 2SF
- Derby City Hospital, Derby DE22 3NE
- Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia, Philadelphia, PA 19104-4399, USA
- Department of Medicine, University of Auckland, Auckland 1001, New Zealand
- Division of Nutritional Biochemistry, University of Nottingham, School of Biosciences, Loughborough LE12 5RD
EDITOR—Parsons et al highlight the importance of maternal weight on birth weight and future obesity in the offspring.1 They emphasise the importance of genetics and debate the relation between reduced intrauterine growth on future obesity but do not discuss the role of fuel mediated teratogenesis during fetal development.2
Fuel mediated teratogenesis proposes that intrauterine exposure of the fetus of women with diabetes in pregnancy to an excess of fuel (for example, glucose) causes permanent fetal change, leading to malformations, greater birth weight, and an increased risk of developing type 2 diabetes in later life.2 More recently, obesity in the offspring has been included as an outcome of fuel mediated teratogenesis in pregnancies complicated by diabetes. 3 4 However, maternal fuel supply across a population is a continuum, and the criteria for gestational diabetes may not be sufficient to differentiate between a diabetogenic and a non-diabetogenic intrauterine milieu.
We investigated the relation between first trimester body mass index and glycaemia at 36 weeks' gestation and birth weight and umbilical cord insulin concentrations in the pregnancies of 63 Polynesian women without gestational diabetes.5 We found that the greater the maternal body mass index (divided into thirds (<25.0, 25.0-31.7, ≥31.8 kg/m2)) the bigger the baby, the higher the maternal fasting glucose concentration (5.1 (SD 0.6), 5.0 (0.5), 5.3 (0.5) mmol/l; P=0.097), and the higher the geometric mean of the umbilical cord insulin concentration (10.0, 14.0, 14.9 μmol/l; P=0.015). There were no differences across the thirds of body mass index in concentrations of cord leptin or insulin-like growth factor-I.
We hypothesised that increasing maternal obesity is associated with increasing maternal glycaemia, thereby stimulating fetal insulin secretion and raising the potential for obesity in the offspring. As plasma glucose is a continuous variable the relation between glycaemia and the future …
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