Moderate beta-cell ablation triggers synergic compensatory mechanisms even in the absence of overt metabolic disruption.
Commun Biol
; 7(1): 833, 2024 Jul 09.
Article
in En
| MEDLINE
| ID: mdl-38982170
ABSTRACT
Regeneration, the ability to replace injured tissues and organs, is a phenomenon commonly associated with lower vertebrates but is also observed in mammals, in specific tissues. In this study, we investigated the regenerative potential of pancreatic islets following moderate beta-cell loss in mice. Using a rapid model of moderate ablation, we observed a compensatory response characterized by transient inflammation and proliferation signatures, ultimately leading to the recovery of beta-cell identity and function. Interestingly, this proliferative response occurred independently of inflammation, as demonstrated in ablated immunodeficient mice. Furthermore, exposure to high-fat diet stimulated beta-cell proliferation but negatively impacted beta-cell function. In contrast, an equivalent slower ablation model revealed a delayed but similar proliferative response, suggesting proliferation as a common regenerative response. However, high-fat diet failed to promote proliferation in this model, indicating a differential response to metabolic stressors. Overall, our findings shed light on the complex interplay between beta-cell loss, inflammation, and stress in modulating pancreatic islet regeneration. Understanding these mechanisms could pave the way for novel therapeutic strategies based on beta-cell proliferation.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Regeneration
/
Cell Proliferation
/
Insulin-Secreting Cells
/
Diet, High-Fat
Limits:
Animals
Language:
En
Journal:
Commun Biol
Year:
2024
Document type:
Article
Affiliation country:
Noruega