AI Article Synopsis
- * Researchers observed a significant increase in β-cell mass in a mouse model of obesity caused by excessive calorie intake, identifying Sin3a as a key regulator in this process through RNA sequencing.
- * Mice lacking Sin3a specifically in their β-cells developed severe diabetes, indicating that Sin3a is crucial for developing β-cell mass after birth and opening up new avenues for understanding β-cell adaptation mechanisms.
Article Abstract
The increase of functional β-cell mass is paramount to maintaining glucose homeostasis in the setting of systemic insulin resistance and/or augmented metabolic load. Understanding compensatory mechanisms that allow β-cell mass adaptation may allow for the discovery of therapeutically actionable control nodes. In this study, we report the rapid and robust β-cell hyperplasic effect in a mouse model of overfeeding-induced obesity (OIO) based on direct gastric caloric infusion. By performing RNA sequencing in islets isolated from OIO mice, we identified Sin3a as a novel transcriptional regulator of β-cell mass adaptation. β-Cell-specific Sin3a knockout animals showed profound diabetes due to defective acquisition of postnatal β-cell mass. These findings reveal a novel regulatory pathway in β-cell proliferation and validate OIO as a model for discovery of other mechanistic determinants of β-cell adaptation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9630089 | PMC |
| http://dx.doi.org/10.2337/db22-0306 | DOI Listing |
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