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The effects of the Pro12Ala polymorphism of the PPAR?-2 gene on lipid metabolism interact with body size at birth

Record type: Article

Body size at birth is an indicator of the intrauterine environment. The effects of the Pro12Pro genotype and the 12Ala allele of the PPAR?-2 gene on glucose and insulin metabolism in adult life depend on body size at birth. A low birth weight is associated with insulin resistance and type 2 diabetes. The peroxisome proliferator-activated receptor-? (PPAR?s) are also regulators of adipocyte differentiation, and the PPAR?-2 gene could also contribute to the development of dyslipidemia. Therefore, the effects of the Pro12Ala polymorphisms of the PPAR?-2 gene on lipid metabolism were measured in 476 elderly persons whose birth weight was known. The Ala12 allele was associated with increased serum total, low-density lipoprotein (LDL), and non-high-density lipoprotein (non-HDL) cholesterol concentrations but only among those who had birth weights below 3000 g. These interactions between the effects of the PPAR?-2 gene on adult traits and the effects of birth weight may be interpreted as examples of gene–environmental interactions, which underlie plasticity during development.

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Citation

Eriksson, J., Lindi, V., Uusitupa, M., Forsen, T., Laakso, M., Osmond, C. and Barker, D. (2003) The effects of the Pro12Ala polymorphism of the PPAR?-2 gene on lipid metabolism interact with body size at birth Clinical Genetics, 64, (4), pp. 366-370. (doi:10.1034/j.1399-0004.2003.00150.x).

More information

Published date: 2003
Keywords: birth weight, developmental plasticity, dyslipidemia, gene-enviroment interaction, ppar?-2gene

Identifiers

Local EPrints ID: 25466
URI: http://eprints.soton.ac.uk/id/eprint/25466
ISSN: 0009-9163
PURE UUID: d05e0d00-22cc-429b-8c2c-10f675d191ec
ORCID for C. Osmond: ORCID iD orcid.org/0000-0002-9054-4655

Catalogue record

Date deposited: 19 Apr 2006
Last modified: 17 Jul 2017 16:10

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Contributors

Author: J. Eriksson
Author: V. Lindi
Author: M. Uusitupa
Author: T. Forsen
Author: M. Laakso
Author: C. Osmond ORCID iD
Author: D. Barker

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