title: A role for sphingolipids in the pathophysiology of obesity-induced inflammation.
abstract: Following the initial discovery that adipose tissue actively synthesizes and secretes cytokines, obesity-induced inflammation has been implicated in the etiology of a host of disease states related to obesity, including cardiovascular disease and type II diabetes. Interestingly, a growing body of evidence similarly implicates sphingolipids as prime instigators in these same diseases. From the recent discovery that obesity-related inflammatory pathways modulate sphingolipid metabolism comes a novel perspective—sphingolipids may act as the dominant mediators of deleterious events stemming from obesity-induced inflammation. This paradigm may identify sphingolipids as an effective target for future therapeutics aimed at ameliorating diseases associated with chronic inflammation.
authors.affiliation: Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA. benjamin_bikman@byu.edu
authors.forename: Benjamin T
authors.initials: BT
authors.lastname: Bikman
mesh_terms: D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism*; D002518:Ceramides / Q000096:biosynthesis; D016207:Cytokines / Q000378:metabolism; D005234:Fatty Liver / Q000209:etiology / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology*; D008954:Models, Biological; D065626:Non-alcoholic Fatty Liver Disease; D009765:Obesity / Q000150:complications*; D015398:Signal Transduction / Q000502:physiology; D013107:Sphingolipids / Q000378:metabolism*; D051197:Toll-Like Receptor 4 / Q000378:metabolism
chemical_list: D002518:Ceramides; D016207:Cytokines; D013107:Sphingolipids; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4