The University of Southampton
University of Southampton Institutional Repository

The effects of the Pro12Ala polymorphism of the peroxisome proliferator–activated receptor-2 gene on glucose/Insulin metabolism interact with prenatal exposure to famine

de Rooij, Susanne R., Painter, Rebecca C., Phillips, David I.W., Osmond, Clive, Tanck, Michael W.T., Defesche, Joep C., Bossuyt, Patrick M.M., Michels, Robert P.J., Bleker, Otto P. and Roseboom, Tessa J. (2006) The effects of the Pro12Ala polymorphism of the peroxisome proliferator–activated receptor-2 gene on glucose/Insulin metabolism interact with prenatal exposure to famine Diabetes Care, 29, (5), pp. 1052-1057. (doi:10.2337/dc05-1993).

Record type: Article


OBJECTIVE: An adverse fetal environment may permanently modify the effects of specific genes on glucose tolerance, insulin secretion, and insulin sensitivity. In the present study, we assessed a possible interaction of the peroxisome proliferator-activated receptor (PPAR)-gamma2 Pro12Ala polymorphism with prenatal exposure to famine on glucose and insulin metabolism.
RESEARCH DESIGN AND METHODS: We measured plasma glucose and insulin concentrations after an oral glucose tolerance test and determined the PPAR-gamma2 genotype among 675 term singletons born around the time of the 1944-1945 Dutch famine.
RESULTS: A significant interaction effect between exposure to famine during midgestation and the PPAR-gamma2 Pro12Ala polymorphism was found on the prevalence of impaired glucose tolerance and type 2 diabetes. The Ala allele of the PPAR-gamma2 gene was associated with a higher prevalence of impaired glucose tolerance and type 2 diabetes but only in participants who had been prenatally exposed to famine during midgestation. Similar interactions were found for area under the curve for insulin and insulin increment ratio, which were lower for Ala carriers exposed to famine during midgestation.
CONCLUSIONS: The effects of the PPAR-gamma2 Pro12Ala polymorphism on glucose and insulin metabolism may be modified by prenatal exposure to famine during midgestation. This is possibly due to a combined deficit in insulin secretion, as conferred by pancreatic beta-cell maldevelopment and carrier type of the Ala allele in the PPAR-gamma2 gene.

Full text not available from this repository.

More information

Published date: 2006
Keywords: aged, alanine, blood, blood glucose, design, diabetes, DNA primers, environment, epidemiology, exposure, female, fetal, genetics, genotype, glucose, glucose tolerance, glucose tolerance test, humans, insulin, male, maternal age, metabolism, methods, netherlands, plasma, polymorphism, genetic, PPAR gamma, pregnancy, prenatal exposure delayed effects, prevalence, proline, research support, non-US gov't, starvation, time


Local EPrints ID: 44227
ISSN: 1935-5548
PURE UUID: dfdc6527-803c-49a0-b20e-3404248278a6
ORCID for Clive Osmond: ORCID iD

Catalogue record

Date deposited: 20 Feb 2007
Last modified: 17 Jul 2017 15:15

Export record



Author: Susanne R. de Rooij
Author: Rebecca C. Painter
Author: David I.W. Phillips
Author: Clive Osmond ORCID iD
Author: Michael W.T. Tanck
Author: Joep C. Defesche
Author: Patrick M.M. Bossuyt
Author: Robert P.J. Michels
Author: Otto P. Bleker
Author: Tessa J. Roseboom

University divisions

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton:

ePrints Soton supports OAI 2.0 with a base URL of

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.