Presentation Title

Characterization of Vitamin D Signaling in INS-1 Pancreatic β-cells

Project Collaborators

Dhananjay Gupta (Collaborating Mentor)

Abstract

Type 2 diabetes (T2D) has emerged as a major public health problem in the US and worldwide. T2D is a multifactorial progressive metabolic disorder where loss of insulin producing β-cells under metabolic stress appears to be the main pathological contributor. Vitamin D [(VitD: [25 (OH)D]) is an essential nutritional component required for normal bone health, optimal functioning of immune system, and metabolism. VitD deficiency has been postulated to be an environmental stressor that increases the risk of developing T2D, however, the molecular regulations of VitD signaling in the pancreatic β-cells are not resolved. A fundamental understanding for effective use of VitD as nutritional supplement is critical for future translational studies and clinical management of T2D. The cellular actions of active VitD are mediated by VitD receptor (VDR) that is abundantly expressed in β-cells. The central theme of the current research project was to evaluate impact of metabolic stress of hyperglycemia on the VitD/VDR signaling on the pancreatic β-cells. The INS-1 β-cells were incubated under normal glucose (5 mM) and hyperglycemic (20 mM) conditions with and without active VitD (10 nM) supplimentations for 48 hr. The VitD treatment under normal glucose environment compared to normal glucose group, significantly (P< 0.05) increased expression of β-cell pro-function and survival marker gene pancreatic and duodenal homeobox 1 (Pdx1), VDR, glucose transporter Glut2 and glucose sensing gene glucokinase (Gck). Under hyperglycemic environment, we observed significant (P

Primary Faculty Mentor Name

Dhananjay (Jay) Gupta

Status

Undergraduate

Student College

College of Agriculture and Life Sciences

Program/Major

Microbiology

Primary Research Category

Biological Sciences

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Characterization of Vitamin D Signaling in INS-1 Pancreatic β-cells

Type 2 diabetes (T2D) has emerged as a major public health problem in the US and worldwide. T2D is a multifactorial progressive metabolic disorder where loss of insulin producing β-cells under metabolic stress appears to be the main pathological contributor. Vitamin D [(VitD: [25 (OH)D]) is an essential nutritional component required for normal bone health, optimal functioning of immune system, and metabolism. VitD deficiency has been postulated to be an environmental stressor that increases the risk of developing T2D, however, the molecular regulations of VitD signaling in the pancreatic β-cells are not resolved. A fundamental understanding for effective use of VitD as nutritional supplement is critical for future translational studies and clinical management of T2D. The cellular actions of active VitD are mediated by VitD receptor (VDR) that is abundantly expressed in β-cells. The central theme of the current research project was to evaluate impact of metabolic stress of hyperglycemia on the VitD/VDR signaling on the pancreatic β-cells. The INS-1 β-cells were incubated under normal glucose (5 mM) and hyperglycemic (20 mM) conditions with and without active VitD (10 nM) supplimentations for 48 hr. The VitD treatment under normal glucose environment compared to normal glucose group, significantly (P< 0.05) increased expression of β-cell pro-function and survival marker gene pancreatic and duodenal homeobox 1 (Pdx1), VDR, glucose transporter Glut2 and glucose sensing gene glucokinase (Gck). Under hyperglycemic environment, we observed significant (P