A histological characteristic of chronic alcoholic pancreatitis is pancreatic fibrosis. In fact, the histological findings show fibrosis, atrophy of the pancreatic acini, chronic inflammation, distortion of the pancreatic ducts with areas of stenosis and characteristic destruction of insulin-producing cells (b cells) and glucagon-producing cells (a cells) (Witt et al.).
Otsuki, "Role of TGF-[beta]1 in the development of pancreatic fibrosis in Otsuka Long-Evans Tokushima Fatty rats," American Journal of Physiology--Gastrointestinal and Liver Physiology, vol.
The involvement of PSCs in pancreatic fibrosis in response to chronic inflammation or pancreatic cancer is well established [8-10, 26-30], but there have been many fewer studies into their potential role in islet fibrosis and progressive [beta]-cell failure in T2DM.
Furthermore, a new era in the understanding of the pathophysiological mechanisms of scar tissue formation in the pancreas (i.e., pancreatic fibrosis) has dawned with the recent identification and culture of pancreatic stellate cells (PSCs), the key effector cells in fibrogenesis.