The hormone-sensitive lipase i6 gene polymorphism and body fat accumulation
Background The hormone sensitive lipase (HSL) catalyses the breakdown of adipose tissue triglycerides into free fatty acids. The objective of this study was to determine whether HSLi6 microsatellite allele 5 (A5) and/or homozygosity for this allele is associated with body fat in Swedes. Design A lar...
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Published in | European journal of clinical investigation Vol. 32; no. 12; pp. 938 - 942 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Science Ltd
01.12.2002
Blackwell Blackwell Publishing Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | Background The hormone sensitive lipase (HSL) catalyses the breakdown of adipose tissue triglycerides into free fatty acids. The objective of this study was to determine whether HSLi6 microsatellite allele 5 (A5) and/or homozygosity for this allele is associated with body fat in Swedes.
Design A large case–control study on gender‐specific association for several body fat‐related clinical parameters to HSLi6 A5, and to HSLi6 A5 homozygosity, comparing A5 with the other alleles in group. The subjects were 323 obese patients (85 males, 238 females) without other metabolic complication, and 301 nonobese healthy individuals (134 males, 167 females). They were analyzed for various body fat‐related clinical parameters, and HSLi6 genotype.
Results Homozygosity for HSLi6 A5 was a risk factor for obesity, BMI ≥ 30 kg m−2 (Odds ratio = 1·75, 95% CI 1·58–1·93) and body fat mass > 39·6% (Odds ratio = 1·89, 95% CI 1·60–2·23) in women. This genotype was also associated with increased diastolic blood pressure and triglyceride level among nonobese women, and with increased body fat mass and waist/hip ratio among nonobese men.
Conclusion HSLi6 A5 homozygosity is a risk factor for body fat accumulation. |
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Bibliography: | ArticleID:ECI1075 ark:/67375/WNG-NFWPJ0HH-L istex:AA2FA2ED0944F2D8B279C224A1E571F956C8869B Center for Molecular Medicine, Department of Molecular Medicine, Karolinska Institutet, at Karolinska Hospital, L8 : 00, 171 76 Stockholm, Sweden (C. Lavebratt, M. Schalling, S. Sengul, S. Ahlberg); Department of Medicine, Karolinska Institutet and Research Center at CME, Huddinge University Hospital, 141 86 Stockholm, Sweden (M. Rydén, J. Hoffstedt). ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0014-2972 1365-2362 |
DOI: | 10.1046/j.1365-2362.2002.01075.x |