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

Document Type : Original Article

Authors

The Departments of Physiology*, Medical Biochemistry & Molecular Biology** and Medical Histology***, Faculty of Medicine, Cairo University

Abstract

Abstract
Background: Disrupting fetal environment in particular the state of hyperglycemia during the critical period of pan-creatic development is one of potential factors that could alter ß-cell function and morphology in adulthood. Vitamin D intake could protect (3-cells from functional impairment and islet cells death.
Aim of Study: Present study aimed to study effect of maternal hyperglycemia on genes regulating insulin-secreting cells development and possible modulating actions of vitamin
D supplementation either during pregnancy or further contin-uation 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 sub-jected 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 Ngn3which 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 ß-cells, enhance insulin secretion and protect against HFD-induced insulinitis.

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