title: Sphingolipids metabolism in the salivary glands of rats with obesity and streptozotocin induced diabetes.
abstract: 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).
authors.affiliation: Department of Hygiene, Epidemiology and Ergonomics, Medical University of Bialystok, Bialystok, Poland.
authors.forename: Marta
authors.initials: M
authors.lastname: Garbowska
authors.affiliation: Department of Physiology, Medical University of Bialystok, Bialystok, Poland.
authors.forename: Bartłomiej
authors.identifier: http://orcid.org/0000-0002-4954-3431
authors.initials: B
authors.lastname: Łukaszuk
authors.affiliation: Department of Physiology, Medical University of Bialystok, Bialystok, Poland.
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Mikłosz
authors.affiliation: Department of Gastroenterology and Internal Medicine, Medical University of Bialystok, Bialystok, Poland.
authors.forename: Igor
authors.initials: I
authors.lastname: Wróblewski
authors.affiliation: Department of Gastroenterology and Internal Medicine, Medical University of Bialystok, Bialystok, Poland.
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Kurek
authors.affiliation: Department of Conservative Dentistry, Medical University of Bialystok, Bialystok, Poland.
authors.forename: Lucyna
authors.initials: L
authors.lastname: Ostrowska
authors.affiliation: Department of Physiology, Medical University of Bialystok, Bialystok, Poland.
authors.forename: Adrian
authors.initials: A
authors.lastname: Chabowski
authors.affiliation: Department of Hygiene, Epidemiology and Ergonomics, Medical University of Bialystok, Bialystok, Poland.
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Żendzian-Piotrowska
authors.affiliation: Department of Conservative Dentistry, Medical University of Bialystok, Bialystok, Poland.
authors.forename: Anna
authors.initials: A
authors.lastname: Zalewska
mesh_terms: D000818:Animals; D002518:Ceramides / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000378:metabolism*; D003922:Diabetes Mellitus, Type 1 / Q000139:chemically induced / Q000378:metabolism*; D059305:Diet, High-Fat; D007333:Insulin Resistance; D008246:Lysophospholipids / Q000378:metabolism; D008297:Male; D009765:Obesity / Q000150:complications / Q000378:metabolism*; D010306:Parotid Gland / Q000378:metabolism*; D017853:Phosphotransferases (Alcohol Group Acceptor) / Q000378:metabolism; D017208:Rats, Wistar; D015398:Signal Transduction; D013107:Sphingolipids / Q000378:metabolism*; D013108:Sphingomyelin Phosphodiesterase / Q000378:metabolism; D013110:Sphingosine / Q000031:analogs & derivatives / Q000378:metabolism; D051049:Sphingosine N-Acyltransferase / Q000378:metabolism; D013311:Streptozocin; D013363:Submandibular Gland / Q000378:metabolism*; D000099157:Sphingosine Kinase
chemical_list: D002518:Ceramides; D008246:Lysophospholipids; D017853:Phosphotransferases (Alcohol Group Acceptor); D013107:Sphingolipids; D013108:Sphingomyelin Phosphodiesterase; D013110:Sphingosine; D051049:Sphingosine N-Acyltransferase; D013311:Streptozocin; D000099157:Sphingosine Kinase; C060506:sphingosine 1-phosphate
keywords: ceramide; insulin resistance; salivary glands; sphingolipids; type 1 diabetes