title: Changes in fat mass after initiation of maintenance dialysis is influenced by the uncoupling protein 2 exon 8 insertion/deletion polymorphism.
abstract: BACKGROUND
  A high body mass index (BMI) has been reported to confer a survival advantage in end-stage renal disease (ESRD) patients. On the other hand, body fat accumulation, especially visceral adipose tissue, is an important risk factor for cardiovascular disease, as well as a clinically important source of adipokines. Uncoupling protein 2 (UCP2) uncouples respiration from ATP synthesis, thus regulating energy expenditure and fat oxidation. In this longitudinal cohort study, we investigated the impact of the UCP2 insertion/deletion (ins/del) polymorphism on body composition changes in ESRD patients starting dialysis.
  
  
  METHODS
  A total of 222 incident Caucasian ESRD patients (mean age 53 +/- 12 years; 60% males) were investigated close to the start of dialysis with peritoneal dialysis (PD; n = 126) or haemodialysis (HD; n = 96), and again after about 1 year (n = 159). Genotyping of the UCP2 ins/del polymorphism was performed in the patients and in 207 healthy controls. Dual-energy X-ray absorptiometry was conducted at baseline and after 1 year to monitor body composition.
  
  
  RESULTS
  While HD patients and PD patients with the ins/del genotype did not display any changes in body composition, the 48 PD patients with the del/del genotype that completed follow-up had a significant increase; DeltaBMI (0.7 +/- 1.8 kg/m(2)), Deltabody fat mass (3.5 +/- 3.8 kg) and Deltatruncal fat mass (1.7 +/- 1.2 kg). In a multiple linear regression analysis, the del/del genotype was an independent predictor of the increase in truncal fat mass in PD patients (F-ratio = 7.99, P < 0.05) together with age and diabetes mellitus.
  
  
  CONCLUSIONS
  PD patients, but not HD patients, with the UCP2 del/del genotype showed a significant increase in total and truncal fat mass during the first year of dialysis therapy, suggesting a possible role for UCP2 in dissipating the excess energy of a high-glucose environment.
authors.affiliation: Divisions of Renal Medicine and Baxter Novum, Karolinska Institutet, K-56 Karolinska University Hospital Huddinge, 141 86 Stockholm, Sweden.
authors.forename: Xin
authors.initials: X
authors.lastname: Wang
authors.forename: Jonas
authors.initials: J
authors.lastname: Axelsson
authors.forename: Louise
authors.initials: L
authors.lastname: Nordfors
authors.forename: A Rashid
authors.initials: AR
authors.lastname: Qureshi
authors.forename: Carla
authors.initials: C
authors.lastname: Avesani
authors.forename: Peter
authors.initials: P
authors.lastname: Barany
authors.forename: Martin
authors.initials: M
authors.lastname: Schalling
authors.forename: Olof
authors.initials: O
authors.lastname: Heimbürger
authors.forename: Bengt
authors.initials: B
authors.lastname: Lindholm
authors.forename: Peter
authors.initials: P
authors.lastname: Stenvinkel
mesh_terms: D000273:Adipose Tissue; D000328:Adult; D000368:Aged; D001823:Body Composition; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000378:metabolism; D005091:Exons; D005260:Female; D006801:Humans; D007473:Ion Channels / Q000235:genetics* / Q000502:physiology*; D007676:Kidney Failure, Chronic / Q000235:genetics / Q000628:therapy; D008297:Male; D008875:Middle Aged; D024101:Mitochondrial Proteins / Q000235:genetics* / Q000502:physiology*; D011110:Polymorphism, Genetic; D006435:Renal Dialysis; D000071246:Uncoupling Protein 2
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; C000604389:UCP2 protein, human; D000071246:Uncoupling Protein 2