Environmental stressors that encounter in early-life and cause abnormal fetal and/or neonatal development may increase susceptibility to
non-communicable diseases such as diabetes. Maternal exposure to ambient fine
particulate matter (PM2.5) is associated with various fetal abnormalities, suggesting that it may program offspring's susceptibility to diabetes. In the present study, we therefore examined whether maternal exposure to
diesel exhaust PM2.5 (
DEP), one of the major sources of ambient PM2.5 in urban areas, programs adult offspring's
glucose metabolism. Female C57Bl/6J mice were intratracheally instilled with
DEP or vehicle throughout a 7-wk preconceptional period, gestation, and lactation, and the
glucose homeostasis of their adult male offspring was assessed. Intraperitoneal
glucose tolerance test (IPGTT) revealed that the maternal exposure to
DEP significantly impaired adult male offspring's
glucose tolerance. Unexpectedly, it did not influence their
insulin sensitivity, whereas it significantly decreased their
glucose-induced insulin secretion (GIIS). This deficit in insulin secretion was corroborated by their significant decrease in
arginine-induced insulin secretion. Histological analysis demonstrated that the deficit in insulin secretion was accompanied by the decrease in pancreatic islet and β cell sizes. To differentiate the effects of maternal exposure to
DEP before birth and during lactation, some offspring were cross-fostered once born. We did not observe any significant effect of cross-fostering on the
glucose homeostasis of adult male offspring and the function and morphology of their β cells. Prenatal exposure to
DEP programs the morphology and function of β cells and thus homeostatic regulation of
glucose metabolism in adult male offspring.