The ΔF508 Gene Mutation of Cystic Fibrosis Transmembrane Regulator Protein Leads to a Progressive Decline of Beta-Cell Function in Mice Carrying This Mutation (original) (raw)

The study investigates the impact of the ΔF508 gene mutation of the cystic fibrosis transmembrane regulator (CFTR) protein on pancreatic beta-cell function in mice. The findings reveal that male and female mice carrying the ΔF508 mutation initially exhibit improved glucose tolerance and insulin sensitivity. However, a progressive decline in beta-cell function and onset of insulin resistance is observed in older male mutant mice. The research uncovers potential mechanisms linking CFTR mutation to diabetes pathophysiology, suggesting that understanding these alterations could yield insights into cystic fibrosis-related diabetes (CFRD) and its management.