The results from new findings about the molecular mechanisms behind the age-dependent deterioration in β-cell function have been published in Advances in Biological Regulation (formerly Advances in Enzyme Regulation); a journal reporting cutting edge scientific progress on regulation at the molecular level.
Defects in pancreatic β-cell function and survival are key components in type 2 diabetes. Though the molecular mechanisms behind the age-dependent deterioration in β-cell function are not fully understood, our previous studies have indicated that the regulation of cytoplasmic free Ca(2+) concentration may be critical and dependent on the proper function of the mitochondria. By the use of three mouse models, we have been able to present data which suggest that even relatively small, time-dependent changes in β-cell signal-transduction result in compromised insulin release in a diabetic phenotype.