Gestational Diabetes But Not Prepregnancy Overweight Predicts For Cardiometabolic Markers In Offspring Twenty Years Later

Context: Maternal gestational diabetes mellitus (GDM) and prepregnancy overweight/obesity [body mass index (BMI) >= 25 kg/m(2)] might adversely affect offspring cardiometabolic health.Objective: To assess the associations between maternal GDM and prepregnancy overweight/obesity with adult offspring cardiometabolic risk factors.Design: Longitudinal cohort study (ESTER Maternal Pregnancy Disorders Study and the Arvo Ylppo Longitudinal Study).Setting: Province of Uusimaa and Northern Finland.Participants: At a mean age of 24.1 +/- 1.3 years, we classified offspring as offspring of mothers with GDM regardless of the prepregnancy BMI (OGDM; n = 193); normoglycemic mothers with pre pregnancy overweight/obesity (ONO; n = 157); and normoglycemic mothers with prepregnancy BMI <25 kg/m(2) (controls; n = 556).Main Outcome Measures: We assessed the cardiometabolic biomarkers from blood and measured the blood pressure at rest and heart rate.Results: Compared with the controls, the OGDM and ONO groups had greater fasting glucose (1.6%; 95% CI, 0.1% to 3.1%; and 2.3%; 95% CI, 0.5% to 4.3%, respectively) and insulin (12.7%; 95% CI, 4.4% to 21.9%; and 8.7%; 95% CI, 0.2% to 17.8%). These differences attenuated to nonsignificance when adjusted for confounders and/or current offspring characteristics, including BMI or body fat percentage. The OGDM group had lower SHBG (men, 12.4%; 95% CI, 20.2% to 3.9%; women, 33.2%; 95% CI, 46.3% to 16.8%), high-density lipoprotein (-6.6%; 95% CI, 10.9% to 2.2%), and apolipoprotein Al (-4.5%; 95% CI, 7.5% to 1.4%). These differences survived the adjustments. The heart rate and other biomarkers were similar among the groups.Conclusions: Adult offspring of mothers with GDM have increased markers of insulin resistance and a more atherogenic lipid profile. These were only partly explained by confounders or current offspring adiposity. Maternal prepregnancy overweight/obesity was associated with impaired offspring glucose regulation, which was explained by confounders and/or current adiposity.