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      Association of UCP3 Gene –55C>T Polymorphism and Obesity in a Spanish Population

      meta-analysis

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          Abstract

          Background/Aims: The uncoupling protein 3 (UCP3) gene has been suggested as a possible determinant affecting obesity risk given its function in the regulation of energy metabolism. However, available genetic association studies have been inconsistent, which could be attributable to not considering individual lifestyle patterns, such as physical activity, a factor that affects UCP3 expression. The objective of this study was to assess the association between the UCP3 –55C>T polymorphism and the risk of obesity. Methods: Case-control study conducted in a sample of Spanish adults. 157 obese subjects (BMI ≧30) and 150 controls (BMI <25) participated in the study. UCP3 –55C>T polymorphism was identified by the polymerase chain reaction–restriction fragment length polymorphism methodology. Results: The odds ratio (OR) for obesity (95% confidence interval [CI]) according to the presence of UCP 3 gene –55C>T polymorphism (heterozygotes and homozygotes merged together), adjusting for age, sex, and recreational physical activity, was 0.61 (0.37–1.00), p = 0.05. Interestingly, this association was only manifest among those with higher recreational physical activity (OR: 0.46, 95% CI 0.21–0.99, p = 0.05) and not among those with lower physical activity (OR: 0.84, 95% CI 0.41–1.70, p = 0.84). Conclusion: UCP3 –55C>T polymorphism carriers have apparently a lower risk of obesity when taking into consideration recreational energy expenditure. Interestingly, this inverse beneficial association may only occur in people with a high level of physical activity.

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          Association between uncoupling protein polymorphisms (UCP2-UCP3) and energy metabolism/obesity in Pima indians.

          K Walder, R A Norman, R L Hanson … (1998)
          The UCP2-UCP3 gene cluster maps to chromosome 11q13 in humans, and polymorphisms in these genes may contribute to obesity through effects on energy metabolism. DNA sequencing of UCP2 and UCP3 revealed three polymorphisms informative for association studies: an Ala-->Val substitution in exon 4 of UCP2, a 45 bp insertion/deletion in the 3'-untranslated region of exon 8 of UCP2 and a C-->T silent polymorphism in exon 3 of UCP3. Initially, 82 young (mean age = 30 +/- 7 years), unrelated, full-blooded, non-diabetic Pima Indians were typed for these polymorphisms by direct sequencing. The three sites were in linkage disequilibrium ( P 45 years of age were considered, heterozygotes (subjects with the highest sleeping metabolic rate) had the lowest BMI (P = 0.04). The location of the insertion/deletion polymorphism suggested a role in mRNA stability; however, it appeared to have no effect on skeletal muscle UCP2 mRNA levels in a subset of 23 randomly chosen Pima Indians. In conclusion, these results suggest a contribution from UCP2 (or UCP3) to variation in metabolic rate in young Pima Indians which may contribute to overall body fat content later in life.
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            A novel polymorphism in the proximal UCP3 promoter region: effect on skeletal muscle UCP3 mRNA expression and obesity in male non-diabetic Pima Indians.

            E Ravussin, J. Xia, S Snitker … (1999)
            UCP2 and UCP3 are newly discovered uncoupling proteins, which are thought to underlie the variability in energy metabolism in humans. Mutations in the UCP2 and/or UCP3 gene have been associated with sleeping metabolic rate. Recently we reported that skeletal muscle UCP3 mRNA expression was positively correlated with sleeping metabolic rate in Pima Indians. To study whether genetic variation in the promoter region of UCP3 contributed to the variation in expression of UCP3, we screened part of the proximal promoter region for polymorphisms. In the first part of the study, the proximal promoter region of UCP3 was screened by direct sequencing in 24 non-diabetic Pima Indians (range body mass index (BMI): 18-47 kg/m2) (Schrauwen et al. Diabetes 1999; 48: 146-149) and skeletal muscle UCP3 mRNA expression was measured by RT-PCR. In the second part of the study, we typed the polymorphism found in the first part of the study in 67 Pima Indians (32 males, 35 females) from the upper and lower extremes of the BMI distribution. We identified a novel C to T substitution in the UCP3 promoter, 6bp upstream of the putative TATA signal, and 55bp upstream of the transcription starting site. Among 18 male subjects, skeletal muscle UCP3 mRNA expression was significantly higher in the C/T & T/T group compared to the C/C homozygotes (P<0.02). However, in the group of 67 Pima Indians genotype frequencies were not different in the obese and lean groups. We identified a novel polymorphism in the proximal promoter region of UCP3, which was associated with increased skeletal muscle expression of UCP3 in male non-diabetic Pima Indians. Considering the suggested role of UCP3 in energy metabolism, this polymorphism might be of physiological importance in the regulation of energy balance.
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              A genetic variation in the 5' flanking region of the UCP3 gene is associated with body mass index in humans in interaction with physical activity.

              K Clement, Laszlo Grand, F Vasseur … (2000)
              In obese French Caucasian subjects we previously described a silent UCP3 Tyr99Tyr mutation, associated with body mass index. We hypothesised that an unknown polymorphism in the vicinity of the gene could contribute to obesity. Morbidly obese subjects were screened for mutations in 1 kb upstream from the UCP3 gene. Association studies were done between a variant and obesity in 401 morbidly obese and 231 control subjects. We detected three rare genetic variants and one polymorphism: a +5 G-->A in exon 1, a -155 C-->T, a -439 A insertion and a -55 C-->T located 6 bp from the putative TATA box. This variant was in linkage disequilibrium with the Tyr99Tyr polymorphism. Frequencies of the variant allele at the -55 locus were similar in the obese and control groups (0.23 vs 0.21). The -55 polymorphism was associated with BMI in the obese group (p = 0.0031): BMI was higher in TT than in CC or CT patients. Likewise control subjects with a TT genotype had a higher BMI (p = 0.03). In the obese group, homozygosity for this variant is a risk factor for high BMI (odds ratio: 1:75, p = 0.02). Obese patients were divided into tertiles according to physical activity. In the group with a wild C/C genotype, BMI was negatively associated with physical activity (p = 0.015). The C-->T polymorphism in the 5' sequences of the UCP3 gene might contribute to the corpulence in obese and normal weight subjects and alter the benefit of physical activity. The UCP3 gene can be considered as a gene modifying corpulence.
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                Author and article information

                Journal
                Journal ID (publisher-id): ANM
                Journal ID (nlm-ta): Ann Nutr Metab
                Journal ID (doi): 10.1159/issn.0250-6807
                Title: Annals of Nutrition and Metabolism
                Publisher: S. Karger AG
                ISSN (Print): 0250-6807
                ISSN (Electronic): 1421-9697
                Publication date Subscription-year: 2005
                Publication date (Print): June 2005
                Publication date (Electronic): 10 August 2005
                Volume: 49
                Issue: 3
                Pages: 183-188
                Affiliations
                Departments of aPreventive Medicine and Public Health, and bPhysiology and Nutrition, University of Navarra, and cService of Endocrinology, Hospital of Navarra, Pamplona, Spain
                Article
                Publisher ID: 86883 Other ID: Ann Nutr Metab 2005;49:183–188
                DOI: 10.1159/000086883
                PubMed ID: 16006788
                SO-VID: 7821a05b-b369-4533-9268-189527bb7e7e
                Copyright © © 2005 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 05 June 2004
                Date accepted : 16 February 2005
                Page count
                Tables: 4, References: 22, Pages: 6
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Nutrition & Dietetics,Health & Social care,Public health
                Keywords: Physical activity,Association studies,Uncoupling protein 3,Obesity
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics, Health & Social care, Public health
                Keywords: Physical activity, Association studies, Uncoupling protein 3, Obesity

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