Impact of Acute Pancreatic Injury on Sphingolipid Metabolism in the Salivary Glands

Abstract

Acute pancreatic injury can be related to both parenchymal (responsible for exocrine functions) and islet (mainly β-cells, responsible for endocrine functions) damage. During embryonic development, both the salivary glands and the pancreas originate from the foregut, which explains many of the observed histological and functional similarities between these two organs. The relationship between several diseases of the pancreas and salivary glands, resulting from morphological and functional similarities, is well established. Sphingolipids constitute a class of biologically active molecules involved in numerous physiological and pathological processes, including acute pancreatitis (AP) and diabetes mellitus. However, the effect of AP on sphingolipid metabolism in the salivary glands remains uncertain. In the presented study, we examined the effect of AP and type 1 diabetes mellitus on sphingolipid metabolism in the salivary glands of rats. We demonstrated that acute pancreatic injury, related to both exocrine and endocrine functions, affects the metabolism of sphingolipids in the parotid, but not submandibular, salivary glands.