Published online before print October 9, 2006, doi: 10.1161/CIRCULATIONAHA.106.625848
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(Circulation. 2006;114:1687-1692.)
© 2006 American Heart Association, Inc.
Epidemiology |
Low Birth Weight, a Risk Factor for Cardiovascular Diseases in Later Life, Is Already Associated With Elevated Fetal Glycosylated Hemoglobin at Birth
From the Center for Cardiovascular Research/Institute of Pharmacology (T.P., M.G., B.H.), Department of Nephrology (T.P., T.S.), Department of Obstetrics and Gynecology (H.H.), and Institute of Laboratory Medicine (F.P.), Charité, Berlin, Germany.
Correspondence to Professor Dr Berthold Hocher, Center for Cardiovascular Research/Institute of Pharmacology, Charité Mitte, Hessische Straße 3-4, 10115 Berlin, Germany. E-mail berthold.hocher{at}charite.de
Received March 8, 2006; revision received August 15, 2006; accepted August 17, 2006.
Background— It remains unclear whether the association between low birth weight and insulin resistance in adulthood has its origin in utero or whether it develops later in life depending on predisposition and exogenous factors.
Methods and Results— Total glycosylated hemoglobin (TGH) was quantified at delivery in 1295 mother/child pairs serving as a surrogate of maternal and fetal glycemia. Multivariable regression analysis considering gestational age at delivery, the child’s sex, maternal body mass index, and smoking during pregnancy revealed that an increase in TGH by 1% in the child was significantly associated with a mean birth weight reduction of 135 g (P<0.0001), whereas the same increase in the mother was associated with a mean birth weight increase of 88 g (P<0.0001). The ratio of fetal/maternal TGH suggests that lighter newborns have a higher percentage of TGH than would be expected from maternal TGH.
Conclusions— The study demonstrates for the first time in a large population that there is an inverse association between TGH of a newborn and its birth weight. This might be due to increased insulin resistance in newborns with lower birth weight. Our data suggest that the pathophysiological mechanisms linking prenatal growth and postnatal sensitivity to insulin are present as early as before birth.
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