title: Visfatin is increased in chronic kidney disease patients with poor appetite and correlates negatively with fasting serum amino acids and triglyceride levels.
abstract: OBJECTIVE
  Anorexia is a common complication of chronic kidney disease (CKD), while novel animal and human data suggest a role for visfatin in regulating feeding behavior. We hypothesized that increased visfatin levels in CKD patients may be involved in the regulation of appetite and nutrient homeostasis.
  
  
  METHODS
  This is a cross-sectional study where circulating visfatin levels were analysed in 246 incident CKD stage 5 patients starting dialysis therapy. The associations between visfatin (enzyme-linked immunosorbent assay, ELISA) and anthropometric and biochemical nutritional status, self-reported appetite, fasting serum amino acids (high-performance liquid chromatography) and circulating cytokine levels (ELISAs) were assessed. We also performed genotyping (Pyrosequencing(R)) of two polymorphisms (rs1319501 and rs9770242) in the visfatin gene.
  
  
  RESULTS
  Serum visfatin concentrations were not associated with either body mass index or serum leptin. Across groups with worsening appetite, median visfatin levels were incrementally higher (P < 0.05). With increasing visfatin tertiles, patients proved to be more often anorectic (P < 0.05) and to have incrementally lower serum albumin, cholesterol and triglycerides as well as lower essential and non-essential serum amino acids (P < 0.05 for all). A polymorphism in the visfatin gene was associated with increased circulating visfatin levels and, at the same time, a higher prevalence of poor appetite (P < 0.05 for both).
  
  
  CONCLUSIONS
  Our study suggests novel links between visfatin and anorexia in CKD patients. Based on recent studies, we speculate that high visfatin in CKD patients may constitute a counter-regulatory response to central visfatin resistance in uremia. Future studies should examine a putative role of visfatin as a regulator of nutrient homeostasis in uremia.
authors: Divisions of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden. juan.jesus.carrero@ki.se
authors: Juan J
authors: JJ
authors: Carrero
authors: Anna
authors: A
authors: Witasp
authors: Peter
authors: P
authors: Stenvinkel
authors: Abdul R
authors: AR
authors: Qureshi
authors: Olof
authors: O
authors: Heimbürger
authors: Peter
authors: P
authors: Bárány
authors: Mohamed E
authors: ME
authors: Suliman
authors: Björn
authors: B
authors: Anderstam
authors: Bengt
authors: B
authors: Lindholm
authors: Louise
authors: L
authors: Nordfors
authors: Martin
authors: M
authors: Schalling
authors: Jonas
authors: J
authors: Axelsson
mesh_terms: D000328:Adult; D000368:Aged; D000596:Amino Acids / Q000097:blood*; D001066:Appetite / Q000502:physiology*; D015992:Body Mass Index; D002908:Chronic Disease; D003430:Cross-Sectional Studies; D005247:Feeding Behavior / Q000502:physiology; D005260:Female; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007674:Kidney Diseases / Q000097:blood* / Q000503:physiopathology*; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood* / Q000235:genetics / Q000502:physiology; D011110:Polymorphism, Genetic / Q000235:genetics; D014280:Triglycerides / Q000097:blood*; D014511:Uremia / Q000097:blood / Q000503:physiopathology
chemical_list: D000596:Amino Acids; D020738:Leptin; D014280:Triglycerides; D054409:Nicotinamide Phosphoribosyltransferase