Mitochondrial complex I subunit deficiency promotes pancreatic α-cell proliferation.

ABSTRACT:

Objective

There is strong evidence that mitochondrial DNA mutations and mitochondrial dysfunction play a role in diabetes pathogenesis. The homozygous knock-in mtDNA mutator mouse is a model of premature aging due to the accumulation of mitochondrial DNA mutations. We used this mouse model to investigate the relationship between mitochondrial subunit expression and pancreatic islet cell composition.

Methods

Quadruple immunofluorescence was used to quantify mitochondrial subunit expression (complex I and IV) and cell composition in pancreatic islets from mitochondrial DNA mutator mice (PolgA^mut/mut) and control C57BL/6 mice at 12 and 44 weeks of age.

Results

Mitochondrial complex I subunit expression was decreased in islets from 12 week PolgA^mut/mut

SUBMITTER: Yu X 

PROVIDER: S-EPMC9046450 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature