| Changes in fat mass after initiation of maintenance dialysis is influenced by the uncoupling protein 2 exon 8 insertion/deletion polymorphism. | |
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MedLine Citation:
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PMID: 16982633 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2006-09-17 |
Journal Detail:
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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:
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Created Date: 2006-12-25 Completed Date: 2007-07-03 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8706402 Medline TA: Nephrol Dial Transplant Country: England |
Other Details:
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Languages: eng Pagination: 196-202 Citation Subset: IM |
Affiliation:
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Divisions of Renal Medicine and Baxter Novum, Karolinska Institutet, K-56 Karolinska University Hospital Huddinge, 141 86 Stockholm, Sweden. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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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