Inflammatory Oxidative Stress Compounds Inhibit Insulin Secretion through Rapid Protein Carbonylation.

ABSTRACT: Pancreatic β-cells in pre-type 1 diabetes (T1D) experience stress due to islet inflammation, which accompanies early defects in insulin secretion that precede autoimmune destruction. One product of inflammatory stress is protein carbonylation (PC), brought on by reactive oxygen species (ROS) combining with lipids to produce reactive aldehydes such as 4-hydroxynonenal (4-HNE) that irreversibly modify Cys, His, and Lys sidechains. In this study, we used proteomics to measure patterns of PC in pancreatic islets from 10-week-old pre-diabetic NOD mice and in cultured insulin-secreting cells treated with either 4-HNE or pro-inflammatory cytokines. All three stress conditions increased carbonylation of proteins central to β-cell function including Rab GTPases and other proteins that are essential

SUBMITTER: Saunders EF 

PROVIDER: S-EPMC12330585 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature