Inherent Beta Cell Dysfunction Contributes to Autoimmune Susceptibility.

Citation
Kim, Y. K., et al. “Inherent Beta Cell Dysfunction Contributes To Autoimmune Susceptibility.”. Biomolecules.
Center University of Colorado Denver
Author Yong Kyung Kim, Lori Sussel, Howard W Davidson
Keywords autoimmunity, beta cell, mitochondria, pancreatic islet, type 1 diabetes
Abstract

The pancreatic beta cell is a highly specialized cell type whose primary function is to secrete insulin in response to nutrients to maintain glucose homeostasis in the body. As such, the beta cell has developed unique metabolic characteristics to achieve functionality; in healthy beta cells, the majority of glucose-derived carbons are oxidized and enter the mitochondria in the form of pyruvate. The pyruvate is subsequently metabolized to induce mitochondrial ATP and trigger the downstream insulin secretion response. Thus, in beta cells, mitochondria play a pivotal role in regulating glucose stimulated insulin secretion (GSIS). In type 2 diabetes (T2D), mitochondrial impairment has been shown to play an important role in beta cell dysfunction and loss. In type 1 diabetes (T1D), autoimmunity is the primary trigger of beta cell loss; however, there is accumulating evidence that intrinsic mitochondrial defects could contribute to beta cell susceptibility during proinflammatory conditions. Furthermore, there is speculation that dysfunctional mitochondrial responses could contribute to the formation of autoantigens. In this review, we provide an overview of mitochondrial function in the beta cells, and discuss potential mechanisms by which mitochondrial dysfunction may contribute to T1D pathogenesis.

Year of Publication
2021
Journal
Biomolecules
Volume
11
Issue
4
Date Published
03/2021
ISSN Number
2218-273X
DOI
10.3390/biom11040512
Alternate Journal
Biomolecules
PMID
33808310