title: Soluble CD163 is not increased in visceral fat and steatotic liver and is even suppressed by free fatty acids in vitro.
abstract: Visceral fat differs from subcutaneous fat by higher local inflammation and increased release of IL-6 and free fatty acids (FFA) which contribute to hepatic steatosis. IL-6 has been shown to upregulate the monocyte/macrophage specific receptor CD163 whose soluble form, sCD163, is increased in inflammatory diseases. Here, it was analyzed whether CD163 and sCD163 are differentially expressed in the human fat depots and fatty liver. CD163 mRNA and protein were similarly expressed in paired samples of human visceral and subcutaneous fat, and comparable levels in portal venous and systemic venous blood of liver-healthy controls indicate that release of sCD163 from visceral adipose tissue was not increased. CD163 was also similarly expressed in steatotic liver when compared to non-steatotic tissues and sCD163 was almost equal in the respective sera. Concentrations of sCD163 were not affected when passing the liver excluding substantial hepatic removal/release of this protein. A high concentration of IL-6 upregulated CD163 protein while physiological doses had no effect. However, sCD163 was not increased by any of the IL-6 doses tested. FFA even modestly decreased CD163 and sCD163. The anti-inflammatory mediators fenofibrate, pioglitazone, and eicosapentaenoic acid (EPA) did not influence sCD163 levels while CD163 was reduced by EPA. These data suggest that in humans neither visceral fat nor fatty liver are major sources of sCD163.
authors.affiliation: Department of Internal Medicine I, Regensburg University Hospital, D-93042 Regensburg, Germany.
authors.forename: Sabrina
authors.initials: S
authors.lastname: Bauer
authors.forename: Thomas S
authors.initials: TS
authors.lastname: Weiss
authors.forename: Reiner
authors.initials: R
authors.lastname: Wiest
authors.forename: Doris
authors.initials: D
authors.lastname: Schacherer
authors.forename: Claus
authors.initials: C
authors.lastname: Hellerbrand
authors.forename: Stefan
authors.initials: S
authors.lastname: Farkas
authors.forename: Marcus N
authors.initials: MN
authors.lastname: Scherer
authors.forename: Mirko
authors.initials: M
authors.lastname: Ritter
authors.forename: Gerd
authors.initials: G
authors.lastname: Schmitz
authors.forename: Andreas
authors.initials: A
authors.lastname: Schäffler
authors.forename: Christa
authors.initials: C
authors.lastname: Buechler
mesh_terms: D000368:Aged; D015703:Antigens, CD / Q000096:biosynthesis / Q000276:immunology*; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis / Q000276:immunology*; D002478:Cells, Cultured; D015536:Down-Regulation; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005234:Fatty Liver / Q000276:immunology* / Q000378:metabolism; D005260:Female; D006801:Humans; D050152:Intra-Abdominal Fat / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000276:immunology*; D015854:Up-Regulation; D000098902:CD163 Antigen
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000098902:CD163 Antigen; D005230:Fatty Acids, Nonesterified; D012333:RNA, Messenger; D011956:Receptors, Cell Surface