sphingosine-kinase and Diabetes-Mellitus--Type-1

Diabetes is considered a major public health problem affecting millions of individuals worldwide. Remarkably, scientific reports regarding salivary glands sphingolipid metabolism in diabetes are virtually non-existent. This is odd given the well-established link between the both in other tissues (e.g., skeletal muscles, liver) and the key role of these glands in oral health preservation. The aim of this paper is to examine sphingolipids metabolism in the salivary glands in (pre)diabetes (evoked by high fat diet feeding or streptozotocin). Wistar rats were allocated into three groups: control, HFD-, or STZ-diabetes. The content of major sphingolipid classes in the parotid (PSG) and submandibular (SMSG) glands was assessed via chromatography. Additionally, Western blot analyses were employed for the evaluation of key sphingolipid signaling pathway enzyme levels. No changes in ceramide content in the PSG were found, whereas an increase in ceramide concentration for SMSG of the STZ group was observed. This was accompanied by an elevation in SPT1 level. Probably also sphingomyelin hydrolysis was increased in the SMSG of the STZ-diabetic rats, since we observed a significant drop in the amount of SM. PSG and SMSG respond differently to (pre)diabetes, with clearer pattern presented by the later gland. An activation of sphingomyelin signaling pathway was observed in the course of STZ-diabetes, that is, metabolic condition with rapid onset/progression. Whereas, chronic HFD lead to an inhibition of sphingomyelin signaling pathway in the salivary glands (manifested in an inhibition of ceramide de novo synthesis and accumulation of S1P).

Topics: Animals; Ceramides; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Diet, High-Fat; Insulin Resistance; Lysophospholipids; Male; Obesity; Parotid Gland; Phosphotransferases (Alcohol Group Acceptor); Rats, Wistar; Signal Transduction; Sphingolipids; Sphingomyelin Phosphodiesterase; Sphingosine; Sphingosine N-Acyltransferase; Streptozocin; Submandibular Gland

Pancreatic islet transplantation is a promising clinical treatment for type 1 diabetes, but success is limited by extensive β-cell death in the immediate posttransplant period and impaired islet function in the longer term. Following transplantation, appropriate vascular remodeling is crucial to ensure the survival and function of engrafted islets. The sphingosine kinase (SK) pathway is an important regulator of vascular beds, but its role in the survival and function of transplanted islets is unknown. We observed that donor islets from mice deficient in SK1 (

Topics: Animals; Cell Movement; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Endothelial Cells; Flow Cytometry; Islets of Langerhans; Islets of Langerhans Transplantation; Lysophospholipids; Mice; Mice, Knockout; Neovascularization, Physiologic; Phosphotransferases (Alcohol Group Acceptor); Real-Time Polymerase Chain Reaction; Sphingosine; Transplants