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Offspring exposed to maternal obesity are more likely to develop pancreatic islet dysfunction, but the underlying mechanistic pathway is unclear. We previously reported that fetal rats exposed to in-utero hyperglycemia had decreased fetal β-cell REG3G, and then developed lower β-cell mass and insulin secretion at adulthood. REG3G is reported to bind EXTL3 which initiates heparan sulfate (HS) synthesize important for pancreatic islet integrity. In this study, we sought the delineate the impact of maternal obesity exposure in altering offspring islet Reg3g and HS, and determine how changes in Reg3g and HS alters offspring islet insulin secretion. We hypothesize that exposure to maternal obesity (MatOb) suppresses offspring β-cell REG3G leading to decreased HS affecting β-cell health/function. We induced maternal obesity by feeding female mice western style diet for 4 weeks, while control mice were fed with regular chow. Offspring were evaluated for fat body mass, glucose intolerance, insulin secretion at postnatal day 21 and at 2-month-old. MatOb mouse offspring had increased fat-to-lean ratio and glucose intolerance but no insulin resistance at postnatal day 21, indicating decreased islet function. We performed islet perifusion to measure insulin induced secretion in postnatal day 21 offsprings. We found that male offspring but not female had impaired insulin secretion. In 2-month old offspring fat-to-lean ratio persisted but only males presented glucose intolerance. We found that pancreatic islet Reg3g expression was higher in MatOb females than males. This was accompanied increased HS in pancreatic islets of MatOb females compared to males. All together our data indicates a sex-specific protective role of Reg3g/HS in pancreatic islet function.

SUN-640 Sex-Specific Difference in REG3G Expression Directs the Maintenance of Islet Function in Offspring of Obese Mice