Overview

• Mitochondria in type 2 diabetic β-cells accumulate misfolded proteins because LONP1 levels are markedly reduced
• University of Michigan researchers confirmed that LONP1 activity fails to engage defense systems against damaged mitochondrial proteins in diabetic islet cells
• Mice lacking LONP1 develop hyperglycemia and lose pancreatic β-cells, and reintroducing LONP1 restores normal glucose regulation and cell survival
• The study shifts the focus of β-cell failure from endoplasmic reticulum stress to mitochondrial protein-folding defects as a key driver of cell death
• The team plans to screen for compounds that boost mitochondrial protein refolding or clearance as potential new treatments for type 2 diabetes