Document Detail


Changes in fat mass after initiation of maintenance dialysis is influenced by the uncoupling protein 2 exon 8 insertion/deletion polymorphism.
MedLine Citation:
PMID:  16982633     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Xin Wang; Jonas Axelsson; Louise Nordfors; A Rashid Qureshi; Carla Avesani; Peter Barany; Martin Schalling; Olof Heimbürger; Bengt Lindholm; Peter Stenvinkel
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-09-17
Journal Detail:
Title:  Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association     Volume:  22     ISSN:  0931-0509     ISO Abbreviation:  Nephrol. Dial. Transplant.     Publication Date:  2007 Jan 
Date Detail:
Created Date:  2006-12-25     Completed Date:  2007-07-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8706402     Medline TA:  Nephrol Dial Transplant     Country:  England    
Other Details:
Languages:  eng     Pagination:  196-202     Citation Subset:  IM    
Affiliation:
Divisions of Renal Medicine and Baxter Novum, Karolinska Institutet, K-56 Karolinska University Hospital Huddinge, 141 86 Stockholm, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue*
Adult
Aged
Body Composition
Body Mass Index
Cardiovascular Diseases / metabolism
Exons
Female
Humans
Ion Channels / genetics*,  physiology*
Kidney Failure, Chronic / genetics,  therapy
Male
Middle Aged
Mitochondrial Proteins / genetics*,  physiology*
Polymorphism, Genetic*
Renal Dialysis
Chemical
Reg. No./Substance:
0/Ion Channels; 0/Mitochondrial Proteins; 0/mitochondrial uncoupling protein 2

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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