Session: OR13-Systemic Regulation of Islet Development & Function
Room 304 (Moscone Center)
Maternal diet (HFD vs. CTR) did not alter fetal offspring body weight, glycemia, pancreatic mass, or circulating glucagon levels. HFD offspring displayed decreased circulating C-peptide levels but normal insulin levels, indicative of decreased insulin secretion and a reduction in insulin clearance. Maternal diet had no effect on offspring islet mass, islet proliferation or β-cell mass, but HFD fetal offspring displayed a significant reduction in α-cell mass. Furthermore, HFD exposure in utero resulted in a significant reduction in islet capillary density and sympathetic innervation.
Juvenile animals exposed to both HFD in utero and postweaning displayed an increase in body weight, fasting insulin and insulin secretion during a glucose tolerance test at 1 year of age compared to animals on the CTR diet. HFD consumption during the postweaning period resulted in expansion of both β- and α-cell mass. HFD-fed offspring that had been exposed to the HFD in utero, however, failed to display this expansion in α-cell mass indicating that maternal HFD exposure causes reduced α-cell plasticity. Furthermore, maternal HFD exposure resulted in a significant reduction in islet capillary density in the juvenile offspring. Overall, our results suggest that HFD consumption during pregnancy leads to an adaptive islet response in the α-cell. Furthermore, our data suggest that exposure to a HFD in utero results in impaired islet vascularization in the fetus and that this effect is sustained later in life. Because of the important role of vascularization of the islet in its morphology and function, these data may provide a novel mechanism by which maternal HFD consumption leads to increased risk of type 2 diabetes.
Nothing to Disclose: LP, SMC, AK, DLT, IT, PB, KLG
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