title: Visfatin/PBEF/Nampt and resistin expressions in circulating blood monocytes are differentially related to obesity and type 2 diabetes in humans.
abstract: Low-grade inflammation is important in the development of obesity related pathologies such as insulin resistance and type 2 diabetes, and also cardiovascular disease. Visfatin/PBEF/Nampt and resistin are proinflammatory adipokines secreted from adipocytes, monocytes, and macrophages, and have been linked to atherosclerotic plaque formation, recently. The aim of the present study was to investigate if the expression of these molecules in circulating blood monocytes is altered in obese and/or type 2 diabetic human subjects. Monocytes were isolated by CD14-antibody based magnetic cell sorting from blood samples of 17 lean controls, 20 obese nondiabetic subjects, and 19 obese patients with type 2 diabetes. FACS analysis was performed to test purity of the cell preparations. Expression of the different adipokines was measured by multiplex real-time PCR on RNA-level. Visfatin/PBEF/Nampt was found to be very strongly expressed in monocytes, whereas resistin levels were significantly lower. Furthermore, visfatin/PBEF/Nampt expression was significantly upregulated in obese type 2 diabetic patients, whereas obese nondiabetics exhibited similar levels compared to lean controls, indicating that visfatin/PBEF/Nampt levels are related to type 2 diabetes rather than to obesity. In contrast, resistin expression displayed a different pattern being significantly increased in obese subjects compared to controls but not related to type 2 diabetes. These data suggest a differential role for these two proinflammatory adipokines in linking metabolic diseases to atherosclerosis with visfatin/PBEF/Nampt being more important in patients with type 2 diabetes and resistin in obese but nondiabetic human subjects.
authors.affiliation: Department of Internal Medicine II and Centre of Molecular Medicine, Universität zu Köln, Köln, Germany. matthias.laudes@uk-koeln.de
authors.forename: M
authors.initials: M
authors.lastname: Laudes
authors.forename: F
authors.initials: F
authors.lastname: Oberhauser
authors.forename: D M
authors.initials: DM
authors.lastname: Schulte
authors.forename: S
authors.initials: S
authors.lastname: Freude
authors.forename: R
authors.initials: R
authors.lastname: Bilkovski
authors.forename: J
authors.initials: J
authors.lastname: Mauer
authors.forename: G
authors.initials: G
authors.lastname: Rappl
authors.forename: H
authors.initials: H
authors.lastname: Abken
authors.forename: M
authors.initials: M
authors.lastname: Hahn
authors.forename: O
authors.initials: O
authors.lastname: Schulz
authors.forename: W
authors.initials: W
authors.lastname: Krone
mesh_terms: D000886:Anthropometry; D016207:Cytokines / Q000097:blood* / Q000235:genetics; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications* / Q000201:enzymology / Q000235:genetics; D005260:Female; D005947:Glucose / Q000494:pharmacology; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000150:complications; D007328:Insulin / Q000494:pharmacology; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000201:enzymology*; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood* / Q000235:genetics; D009765:Obesity / Q000097:blood* / Q000150:complications* / Q000201:enzymology / Q000235:genetics; D052243:Resistin / Q000097:blood* / Q000235:genetics
chemical_list: D016207:Cytokines; D007328:Insulin; D018950:Lipopolysaccharide Receptors; D052243:Resistin; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human; D005947:Glucose