Mother‐child cardiometabolic health 4–10 years after pregnancy complicated by obesity with and without gestational diabetes

Abstract

Objective Obesity in pregnancy and gestational diabetes (GDM) increase cardiometabolic disease risk but are difficult to disentangle. This study aimed to test the hypothesis that 4–10 years after a pregnancy complicated by overweight/obesity and GDM (OB‐GDM), women and children would have greater adiposity and poorer cardiometabolic health than those with overweight/obesity (OB) or normal weight (NW) and no GDM during the index pregnancy. Methods In this cross‐sectional study, mother‐child dyads were stratified into three groups based on maternal health status during pregnancy (OB‐GDM = 67; OB = 76; NW = 76). Weight, height, waist and hip circumferences, and blood pressure were measured, along with fasting glucose, insulin, HbA1c, lipids, adipokines, and cytokines. Results Women in the OB and OB‐GDM groups had greater current adiposity and poorer cardiometabolic health outcomes than those in the NW group (p < 0.05). After adjusting for current adiposity, women in the OB‐GDM group had higher HbA1c, glucose, HOMA‐IR and triglycerides than NW and OB groups (p < 0.05). Among children, adiposity was greater in the OB‐GDM versus NW group (p < 0.05), but other indices of cardiometabolic health did not differ. Conclusions Poor cardiometabolic health in women with prior GDM is independent of current adiposity. Although greater adiposity among children exposed to GDM is evident at 4–10 years, differences in cardiometabolic health may not emerge until later.

Obesity and Overweight: Probing Causes, Consequences, and Novel Therapeutic Approaches Through the American Heart Association's Strategically Focused Research Network

“…Children's cardiometabolic traits were modestly correlated with those of their mothers, but at this young age, only adiposity significantly differed across groups, with higher numbers in children exposed to maternal obesity, with and without GD. 49 The lack of group differences on other cardiometabolic biomarkers and traits in children suggests that the perturbations produced by in utero exposure to maternal obesity or GD, as reported in prior studies, 43 , 56 may become more pronounced once children reach puberty or adolescence. Epigenome‐wide association studies in mothers and children demonstrated that several biologically putative genes were associated with cardiometabolic disease phenotypes including STAT3 , SOCS , and AKT , all involved in leptin and insulin signaling, genes regulating inflammatory responses, and genes involved in cellular vesicular trafficking, including intracellular translocation of SLC2A4 , the gene encoding GLUT4 (glucose transporter type 4).…”

“…Note that a full list of all of the articles supported through this center is included within the reference section. 48 , 49 , 50 , 51 , 52 , 53 , 54 Figure 4 summarizes the center's key accomplishments.…”

“…Women with a history of obesity in pregnancy, with and without GD, had a poorer cardiometabolic phenotype as compared with women with normal weight during the index pregnancy. 49 However, the women with obesity were different depending on whether GD was also present. In women with obesity but no GD, poor cardiometabolic health was associated with current adiposity.…”

Leptin resistance in children with in utero exposure to maternal obesity and gestational diabetes

“…The main findings from this parent study have been published. 25 In brief, children exposed to maternal overweight or obesity, with and without GDM, had a greater body mass index z-score (BMIz) and more adiposity than children born to women with normal weight. These children also had slightly higher leptin concentrations than those born to women with normal weight, but the difference did not achieve statistical significance.…”

“…These children also had slightly higher leptin concentrations than those born to women with normal weight, but the difference did not achieve statistical significance. 25 It is possible that no difference was observed because the model did not consider adiposity. The purpose of this new analysis is to explore whether leptin relative to adiposity (i.e., leptin resistance) differs by in utero exposure and whether there is an interaction of in utero exposure with children's current weight status, which may help to explain whether leptin resistance could contribute to the development of obesity in high-risk children.…”