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Horm Res Paediatr. 2010;74(4):267-74. doi: 10.1159/000295710. Epub 2010 May 1.

Insulin resistance, a link between maternal overweight and fetal macrosomia in nondiabetic pregnancies.

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Department of Women's and Children's Health, Uppsala University, Uppsala, Sweden.



During the last decades the number of large for gestational age infants delivered by nondiabetic mothers has increased. Our aim was to investigate to what extent fetal growth in nondiabetic pregnant women can be explained by rates of maternal energy substrate production and resting energy expenditure.


Twenty nonsmoking pregnant women without impaired glucose tolerance and with a wide range of fetal weights (0.2-2.7 SDS) were investigated at 36 weeks of gestation. Maternal lipolysis, glucose production, resting energy expenditure, body composition and insulin resistance were assessed.


Median (range) glucose production rate was 805 (653-1,337) μmol/min and that of glycerol, reflecting lipolysis, was 214 (110-576) μmol/min. Multiple linear regression analysis showed that maternal fat mass explained 36% of the variation in insulin resistance, accounting for 62% of the variation in glucose production. Further, glucose production explained 31% of the variation in fetal weight. Resting energy expenditure explained 51% of the variation in estimated fetal weight.


Fetal weight is dependent on maternal glucose production, which is in turn determined by the degree of insulin resistance, induced in part by the maternal fat mass. The variation in maternal resting energy expenditure is closely related to fetal weight.

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