JNK1 ablation improves pancreatic β-cell mass and function in db/db diabetic mice without affecting insulin sensitivity and adipose tissue inflammation.
hyperglycemia
insulin secretion
kidney
metabolic stress
Journal
FASEB bioAdvances
ISSN: 2573-9832
Titre abrégé: FASEB Bioadv
Pays: United States
ID NLM: 101733210
Informations de publication
Date de publication:
Feb 2021
Feb 2021
Historique:
received:
27
08
2020
revised:
12
12
2020
accepted:
16
12
2020
entrez:
22
2
2021
pubmed:
23
2
2021
medline:
23
2
2021
Statut:
epublish
Résumé
The cJun N-terminal Kinases (JNK) emerged as a major link between obesity and insulin resistance, but their role in the loss of pancreatic β-cell mass and function driving the progression from insulin resistance to type-2 diabetes and in the complications of diabetes was not investigated to the same extent. Furthermore, it was shown that pan-JNK inhibition exacerbates kidney damage in the db/db model of obesity-driven diabetes. Here we investigate the role of JNK1 in the db/db model of obesity-driven type-2 diabetes. Mice with systemic ablation of JNK1 (JNK1
Identifiants
pubmed: 33615154
doi: 10.1096/fba.2020-00081
pii: FBA21192
pmc: PMC7876705
doi:
Types de publication
Journal Article
Langues
eng
Pagination
94-107Informations de copyright
© 2020 The Authors. FASEB BioAdvances published by the Federation of American Societies for Experimental Biology.
Déclaration de conflit d'intérêts
No potential conflict of interest relevant to this article was reported.
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