Vitamin D Supports (3-Cell Remodeling Capacity and Could Reduce High Fat Diet-induced Insulinitis in Pups Born to Diabetic Mothers

ASMAA M. SHAMS EL-DEEN, M.D.; MANAL MOUSTAFA, M.D., MARWA F. AMER, M.D.; GEORGE N. MORCOS, M.D., HANAN ABDALLAH, M.D.
2018 The Medical journal of Cairo University  
Disrupting fetal environment in particular the state of hyperglycemia during the critical period of pancreatic development is one of potential factors that could alter β -cell function and morphology in adulthood. Vitamin D intake could protect β -cells from functional impairment and islet cells death. Aim of the Study: Present study aimed to study effect of maternal hyperglycemia on genes regulating insulin-secreting cells development and possible modulating actions of Vitamin D
more » ... either during pregnancy or further continuation till weaning, also its possible protection from excess dietary fat intake. Methods: Twenty four adult female rats were mated and after confirmation of day 0 pregnancy, six of them were considered as control and the remaining eighteen were subjected to STZ-induced gestational diabetes then subdivided into pregnant-STZ, pregnant-STZ-supplied with Vitamin D during pregnancy and pregnant-STZ-supplied with Vitamin D during pregnancy and lactation till weaning. After weaning, pups born to those mothers were subjected to IPGTT then half of them were sacrificed and the rest were supplied with 45% HFD for two consecutive weeks. Results: The results observed up-regulation of Arx unlike Pax4 and Ngn3 which were down-regulated in pregnant-STZ group together with impairment of IPGTT and reduced area% of insulin immune-reactivity, these changes were augmented secondary to 45% intake of HFD. However, modulating impact of Vitamin D was more obvious in pregnant-STZ-supplied with Vitamin D during pregnancy and lactation than pregnant-STZ-supplied with Vitamin D only during pregnancy. Conclusion: Vitamin D supplementation till time of weaning could affect developmental programming of β -cells, enhance insulin secretion and protect against HFD-induced insulinitis.
doi:10.21608/mjcu.2018.59611 fatcat:rfktre3juvcgdnxtp5u5duzb3a