Mitochondrial complex I subunit deficiency promotes pancreatic α-cell proliferation.
Mitochondria
Pancreatic islets
mtDNA
mtDNA mutator mice
Journal
Molecular metabolism
ISSN: 2212-8778
Titre abrégé: Mol Metab
Pays: Germany
ID NLM: 101605730
Informations de publication
Date de publication:
06 2022
06 2022
Historique:
received:
01
03
2022
accepted:
28
03
2022
pubmed:
8
4
2022
medline:
11
5
2022
entrez:
7
4
2022
Statut:
ppublish
Résumé
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. 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 Mitochondrial complex I subunit expression was decreased in islets from 12 week PolgA Complex I deficiency promotes α-cell proliferation and alters islet cell composition.
Identifiants
pubmed: 35390502
pii: S2212-8778(22)00058-8
doi: 10.1016/j.molmet.2022.101489
pmc: PMC9046450
pii:
doi:
Substances chimiques
DNA, Mitochondrial
0
Electron Transport Complex I
EC 7.1.1.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101489Subventions
Organisme : Wellcome Trust
ID : 203105/Z/16/Z
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/L016354/1
Pays : United Kingdom
Organisme : Biotechnology and Biological Sciences Research Council
Pays : United Kingdom
Informations de copyright
Copyright © 2022 The Authors. Published by Elsevier GmbH.. All rights reserved.
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