Increasing evidence demonstrates that children born to women who consumed a calorically dense, Western-style diet (WSD) during pregnancy are at increased risk of cardiometabolic disease, including Type 2 diabetes.
In a primate (Japanese macaque) model, Maureen Gannon, PhD, and colleagues tested whether exposure to maternal WSD altered the function of the offspring’s insulin-producing beta cells in the pancreatic islets.
They found that prenatal exposure to maternal WSD resulted in programmed changes in fetal islets, and insulin hypersecretion at weaning, that persisted in 3-year-old offspring, even after weaning to a lower-calorie control diet. Insulin-stimulated glucose uptake in skeletal muscle was also reduced in fetal and 1-year-old offspring. In humans, insulin hypersecretion is associated with adverse clinical outcomes of insulin resistance, including increased fat mass and Type 2 diabetes.
Their findings, reported in the American Journal of Physiology-Endocrinology and Metabolism, suggest that islet hyperfunction is programmed by maternal diet, and that changes can be detected as early as the postweaning period in nonhuman primate offspring.
The study was conducted in collaboration with researchers from the University of Oregon and the Oregon National Primate Research Center, the University of Colorado, University of Oklahoma, and Baylor College of Medicine.
Co-authors from Vanderbilt University and Vanderbilt University Medical Center were Darian Carroll, Joseph Elsakr, Allie Miller, and Jennifer Fuhr.
The research was supported in part by National Institutes of Health grants OD011092, DK135164, GM007347, DK090964, DK128187, and DK128416.
