Campbell Miller
Research Mentor(s): Scott Soleimanpour
Mentor Department: Internal Medicine/MEND
Authors:
Session: Session 6 (3:00pm – 3:50pm)
Presentation Type: Poster 41
Abstract
Diabetes mellitus is an increasingly prevalent disease of two primary types, type 1 and 2 diabetes, which affects over 537 million adults worldwide. Type 2 diabetes, the primary focus of this study, is defined as the loss of blood glucose regulation from an impairment in ß-cell function compared to the loss of glucose regulation from an autoimmune attack as defined in type 1 diabetes. Studies have shown that the loss of function in ß-cells in type 2 diabetes can be attributed to defects in their mitochondrial structure. This can be seen specifically with the loss of LONP1, which is an essential protease and protein chaperone in mitochondrial protein quality control and whose function is impaired in humans with type 2 diabetes. Loss of LONP1 in beta cells in mice leads to glucose intolerance. We have also previously observed the mitophagy, which controls the selective disposal of damaged mitochondria, is also disrupted in type 2 diabetes. These potential correlations have led to the hypothesis that mitochondrial protein quality control and mitophagy cooperate to promote ß-cell health. This study will aim to determine the coordinated functions between these two pathways and how the impairment of one or both affects glucose regulation and ß-cell mitochondria health. This will be visualized using physiological studies and histomorphometric analyses of tissue in genetic mouse models. The results of this study are expected to highlight complementary pathways that can be used to protect from loss of function in ß-cells that lead to type 2 diabetes.
