Gestational diabetes exposure in utero tied to higher body fat, energy intake for youths
Key takeaways:
- Exposure to gestational diabetes early in pregnancy is linked to altered hypothalamic glucose response.
- Children born to mothers with gestational diabetes had higher calorie, carbohydrate and sugar intake.
CHICAGO — Children exposed to gestational diabetes in utero have an altered hypothalamic response to glucose, higher energy intake and progressive increases in body fat during childhood, researchers reported.
At the American Diabetes Association Scientific Sessions, researchers presented data from 223 children born in the Kaiser Permanente Southern California health system who were part of the BrainChild cohort. Ella C. Morgan, a research assistant at the Keck School of Medicine of University of Southern California, said the goal of the study was to examine differences in brain data, body composition, dietary habits and other factors between children born to mothers with gestational diabetes and those whose mother did not have gestational diabetes.
Children of mothers with gestational diabetes may have a more rapid increase in body fat percentage than those not exposed to gestational diabetes. Image: Adobe Stock
“We know, based on all of this together, that the gestational diabetes-exposed kids are having a heightened response to glucose in the hypothalamus, the key area in the brain that controls appetite,” Morgan told Healio. “In terms of their eating behavior, they’re consuming more, and that’s mainly driven by increases in sugar intake. In terms of body composition, their body fat change over time, specifically in entrance to puberty, is accelerating.”
Ella C. Morgan
Morgan and colleagues collected data at baseline when children were a mean age of 8.56 years and conducted follow-up assessments 1 year later. Of the study group, 72 children had mothers diagnosed with gestational diabetes after 26 weeks of pregnancy, 40 children had mothers diagnosed with gestational diabetes at 26 weeks or earlier in pregnancy, and 111 children were not exposed to gestational diabetes in utero. Hypothalamic activity was assessed using functional MRI. Body fat was measured and 24-hour dietary recalls conducted at baseline and 1 year.
Children exposed to gestational diabetes early in utero had greater glucose-stimulated activation in the hypothalamus than children not exposed to gestational diabetes (P = .03). There was no difference in glucose-stimulated activation between the group exposed to gestational diabetes late in pregnancy and the control group.
Increased hypothalamic glucose response was tied to a more rapid rise in body fat percentage from baseline to 1 year. Children born to mothers with gestational diabetes had a greater increase in body fat percentage from baseline to 1 year than those not exposed to gestational diabetes.
“We’ll need more data and more analysis to understand the predictive factor here, but I still think that this is a valuable insight to consider that when this hypothalamic response to glucose is altered, it can be a sign to drive or at least be associated with increased body fat,” Morgan said.
Children in both gestational diabetes groups had a higher intake of calories, particularly carbohydrates and simple sugars than the control group. No difference was observed for intake of protein or fiber between the two groups.
The researchers concluded that a neural pathway may be tying gestational diabetes exposure to future metabolic risk. Morgan said more research is needed to examine additional variables, such as physical activity and sleep, to understand how they may impact children exposed to gestational diabetes.
“We’re looking at physical activity to try to understand how this relationship between dietary intake and body fat could potentially be mediated by physical activity or sleep, which could be helpful in lifestyle recommendations for these children,” Morgan said.
For more information:
Kathleen A. Page, MD, associate professor of medicine and co-director of the Diabetes and Obesity Research Institute at the Keck School of Medicine of USC, is the principal investigator and corresponding author of the study. She can be reached at [email protected].
Sources/Disclosures
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Morgan EC, et al. Abstract 2077-LB. Presented at: American Diabetes Association Scientific Sessions; June 20-23, 2025; Chicago.
Disclosures:
The study was supported by the NIH and the American Diabetes Association Pathway Accelerator Award. Morgan reports no relevant financial disclosures.
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