A study results showed that maternal obesity during pregnancy may increase the risk for metabolic compromise in the offspring that is already apparent at birth.
Offspring of obese mothers have an increased risk for obesity and diabetes, write Patrick M. Catalano, MD, from Case Western Reserve University at MetroHealth Medical Center in Cleveland, Ohio, and colleagues. The purpose of this study was to determine whether fetuses of obese women have increased obesity, insulin resistance, and markers of inflammation, supporting the concept of fetal programming.
The study investigated 53 lean and 68 obese women with singleton term pregnancies who were assessed at elective cesarean delivery. The investigators determined measures of insulin resistance and cytokines from maternal blood and umbilical cord blood, and within 24 hours of delivery anthropometric measurements allowed evaluation of neonatal body composition.
Compared with newborns born to lean women, those born to obese women had greater percent body fat (13.1% ± 3.4% vs 11.6% ± 2.9%; P = .02), homeostasis model assessment of insulin resistance (1.51 ± 0.86 vs 1.06 ± 0.70; P = .003), cord leptin (14.5 ± 13.5 ng/mL vs 8.2 ± 4.7 ng/mL; P = .001), and interleukin-6 (3.5 ± 2.3 pg/mL vs 2.4 ± 1.4 pg/mL; P = .02).
Even after adjusting for potential confounders, there was a strong positive correlation between fetal adiposity and insulin resistance (r = .32; P = .0008) as well as maternal pregravid body mass index (BMI) and fetal insulin resistance (r = 0.31; P = .007). Although cord leptin correlated significantly with fetal insulin resistance (r = .30; P = .001), there were no significant correlations between any other umbilical cord cytokines and fetal insulin resistance.
These data suggest that maternal obesity creates a significant risk for the next generations with metabolic compromise already apparent at birth, the study authors write. Therefore, if prevention of obesity is the goal rather than treatment, the perinatal period may be an important focus of future research.
The study showed a drawback that the estimates of insulin resistance in this study are likely to reflect mostly peripheral and not hepatic insulin resistance.
Until we attain a better understanding of the underlying genetic predispositions, physiology and mechanisms relating to maternal and feto-placental interactions, strategies to counteract the epidemic of obesity must by necessity be considered treatment rather than prevention, the study authors conclude.