The variants of the chronic pancreatitis course at diabetes mellitus (possible pathogenetic mechanisms)

Abstract

The article presents analysis of the relationship between the endocrine and exocrine parenchyma of the pancreas, which can result in the development of chronic pancreatitis and diabetes mellitus (in particular, of the «pancreatogenic» type). The latter develops at cystic fibrosis, calcifying pancreatitis, after surgical interventions on the pancreas (due to imbalance between the hormones of the gland). Its clinical diagnostic criteria include exocrine pancreatic insufficiency, chronic pancreatitis signs according to the results of Endo ultrasound, MRI, the absence of type 1 diabetes, decrease of C‑peptide, lack of insulin resistance, impaired secretion of incretins and pancreatic polypeptide.The literature data have been presented on the mechanism of the development of exocrine pancreatic insufficiency at type 1 and type 2 diabetes mellitus, evidencing about the pancreas fibrosis and atrophy due to the development of chronic systemic inflammation, specific for the formation of both chronic pancreatitis and diabetes mellitus. This process at type 2 diabetes mellitus is affected by the decreased trophic effects of insulin on the acinar tissue of the pancreas (due to a decrease in its supply to the acini), autoimmune mechanisms, diabetic and autonomic neuropathy, and molecular signaling pathways. The role of the enzymatic pancreatic insufficiency has been defined in the development and progression of chronic pancreatitis, type 2 diabetes mellitus and metabolic syndrome. Considerations have been given to the mechanisms of the development of liver steatosis, steatohepatitis and diagnostic signs of non‑alcoholic pancreatic fatty disease in the metabolic syndrome, including type 2 diabetes and obesity. Attention has been focused on the role of the acinar‑islet‑acinar axis in the development of steatosis and steato‑pancreatitis. The possibility to provide glucose utilization with insulin‑dependent mechanism (in muscle and adipose tissue) and amylase‑dependent (in the intestine due to the participation of microbiota) has been outlined.