title: Sulfatide increases adiponectin and decreases TNF-alpha, IL-6, and IL-8 in human adipose tissue in vitro.
abstract: Type 2 diabetes is associated with decreased levels of the glycosphingolipid sulfatide, as well as a state of low-grade inflammation. Sulfatide is reported to have anti-inflammatory properties in other cell-types. In the present study, the effects of sulfatide on adipokine (adiponectin, TNF-alpha, IL-6, and IL-8) production in human adipose tissue (AT) was investigated in vitro. Isolated human adipocytes and AT cultures were incubated with sulfatide isolated from pig brain [sulfatide containing a variety of fatty acids or isoforms of sulfatide with defined, saturated fatty acids with 16 (C16:0) or 24 (C24:0) carbon atoms]. Adiponectin production was increased 50-80%, by all sulfatide preparations. Only the C16:0 isoform decreased TNF-alpha, IL-6, and IL-8 production 20-30%. The C16:0 sulfatide has been shown to activate potassium channels in beta-cells, and glibenclamide, an ATP-sensitive K+-(KATP) channel blocker, reversed the C16:0-induced decrement in stimulated TNF-alpha, IL-6, and IL-8 release in adipocytes. Glibenclamide on its own was without effect on the production of adiponectin, TNF-alpha, IL-6, and IL-8. In conclusion, this study shows that, sulfatide exerts anti-inflammatory effects in human adipocytes and AT in vitro. Accordingly, the reported low serum levels of sulfatide in patients with type 2 diabetes might be of importance in relation to the chronic low-grade inflammatory state found in this disease.
authors.affiliation: Department of Endocrinology and Metabolism C, Aarhus University Hospital, Aarhus Sygehus, Tage Hansensgade 2, DK-8000 Aarhus C, Denmark. Jens.Bruun@ki.au.dk
authors.forename: Jens M
authors.initials: JM
authors.lastname: Bruun
authors.forename: Allan
authors.initials: A
authors.lastname: Roeske-Nielsen
authors.forename: Bjørn
authors.initials: B
authors.lastname: Richelsen
authors.forename: Pam
authors.initials: P
authors.lastname: Fredman
authors.forename: Karsten
authors.initials: K
authors.lastname: Buschard
mesh_terms: D017667:Adipocytes / Q000166:cytology / Q000378:metabolism; D052242:Adiponectin / Q000378:metabolism*; D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000328:Adult; D000818:Animals; D002478:Cells, Cultured; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism*; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism*; D009765:Obesity / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013433:Sulfoglycosphingolipids / Q000494:pharmacology*; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*; D014930:Women
chemical_list: D052242:Adiponectin; D015850:Interleukin-6; D016209:Interleukin-8; D012333:RNA, Messenger; D013433:Sulfoglycosphingolipids; D014409:Tumor Necrosis Factor-alpha