Obese women tend to have big babies irrespective of the amount of weight they gain.26 Also, maternal glucose metabolism and adiposity are highly correlated with fetal growth and body composition.21,27 Although gestational age at birth is the strongest predictor of both birth weight and infant fat-free mass, maternal pregravid BMI is the strongest predictor of infant fat mass (r2 = 0.066), explaining about 7% of the variance in body fat of newborns.
Maternal diabetes is a strong predictor of fetal overgrowth, with diabetic women facing a three-fold higher risk of having an LGA baby than obese women. Four times as many LGA infants are born to obese women than to diabetic women because there are many more obese women than diabetic women. Also, diabetic women usually are carefully monitored by their health care providers during pregnancy whereas no special care is provided to obese women. The additional care given to diabetic women undoubtedly reduces the number of LGA babies born to them. Recent studies from both North America and Europe report increases in mean birth weight over the past 30 years.21 This rise in birth weight is likely related to the increasing incidence of maternal obesity. In fact, Catalano and his co-workers in Cleveland, Ohio found that a mean increase in birth weight of 116 g over the past 30 years was more strongly correlated with maternal weight at delivery than any other maternal characteristic.
Is this rise in birth weight linked to an increased maternal subclinical inflammation and insulin resistance associated with obesity? Preliminary data suggest that it may be.28 For example, Radaelli and co-workers29 measured circulating maternal and fetal cytokines and growth factors in three mother-infant cohorts divided into tertiles according to neonatal body fat. The only fetal factor associated with neonatal body fat was leptin (p <0.006), whereas the only maternal factor associated with neonatal body fat was IL-6 (p <0.01). None of the other inflammatory cytokines was elevated in the mothers at delivery. Possibly, the placenta releases some of the mediators of inflammation such as IL-6 into maternal circulation, which in turn blunts maternal insulin action and enhances the fetal fuel supply.
Studies of placenta from lean and obese (>16% body fat) babies showed that the main placental phospholipases were increased in the obese compared to lean infants (p <0.05). Higher levels of phospholipases were associated with increased amounts of omega-3-derived metabolites in the placenta which may in turn modify the membrane lipid biolayers, membrane fluidity, and the efficiency of nutrient transfer. Studies in animals supported the conclusion that phospholipase influences adipose tissue metabolism and glucose tolerance. Mice with phospho-lipase A2 mutations that reduced their adipose tissues had higher levels of insulin sensitivity.30
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