1. ^*Center for Cardiovascular Research/Institute of Pharmacology, Charité, Berlin, Germany;
2. ^†Department of Nephrology, Charité, Berlin, Germany;
3. ^‡Institute of Clinical Biochemistry, Charité, Berlin, Germany;
4. ^§Department of Obstetrics and Gynecology, Charité, Berlin, Germany.

Correspondence: Berthold Hocher Center for Cardiovascular Research/Institute of Pharmacology, Charité Mitte, Hessische Str. 3–4, 10115 Berlin, Germany. E-mail: berthold.hocher@charite.de

^*The costs of publication of this article were defrayed, in part, by the payment of page charges. This article must, therefore, be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 13 December 2005; Accepted 21 August 2006.

Abstract

The association between the peroxisome proliferator-activated receptor (PPAR)2 Pro12Ala polymorphism and insulin resistance is reported to depend on low birth weight. Low birth weight itself has been linked to type 2 diabetes and cardiovascular diseases in adulthood. We assessed whether the PPAR2 Pro12Ala polymorphism determines body size at birth and whether metabolic differences between the genotypes are already detectable in the newborn. This study was conducted at the obstetrics department of the Charité, Berlin, Germany. One thousand nine hundred thirty white woman/child pairs were consecutively included and genotyped. The newborn's weight, length, and head circumference were measured. Total glycated hemoglobin in blood served as a surrogate of fetal insulin resistance and glucose use. We found that neither the fetal nor the maternal Pro12Ala genotype determined body size or total glycated hemoglobin at birth. The results suggest that the PPAR2 Pro12Ala polymorphism is not relevant for intrauterine growth. Previously reported effects of PPAR2 Pro12Ala on insulin resistance seem to arise later in life.