Patients with Type 2 diabetes have constantly elevated blood glucose levels that impair the function of β cells in the pancreas, but the molecular mechanisms involved in this process have remained unclear. In September 15
Maedler et al. exposed islet cells from nondiabetic organ donors to high glucose levels in vitro and observed a release of IL-1β that led to NFκ-B activation, Fas upregulation, DNA fragmentation and impaired β cell function. In addition, they presented in vivo evidence suggesting that IL-1β production is increased in β cells in response to elevated glucose levels.
"The pathway by which hyperglycemia causes impairment and loss of insulin-producing cells thus shares features with immune-mediated processes. It follows that ...
