This study does not show any relationship between the Pro12Ala polymorphism of the PPARgamma gene and fasting FFAs in the general population. The possibility of a different handling of FFAs under different conditions (i.e. postprandial) cannot be excluded and remains to be explored.

OBJECTIVE: To explore the association of the Pro12Ala mutation in the peroxisome proliferator-activated receptor g g g2 with severe obesity and the features of the metabolic syndrome in a population-based sample of Caucasians. PARTICIPANTS AND METHODS: The study is based on a case ± control design: 95 non-diabetic severely obese (body mass index, BMI b 35 kgam 2 ) cases and 280 normal weight (BMI`25 kgam 2 ), age-and sex-matched controls selected from the same population were studied. Height, weight, waist circumference, as well as blood pressure were measured according to a standard protocol. BMI at age 25 y was calculated on the basis of current height and reported weight at age 25 y Biochemical measurements included fasting glucose, triglycerides, high-density lipoprotein cholesterol and insulin. DNA analysis was conducted by PCR and gel electrophoresis. RESULTS: Age and gender distribution were similar in obese and normal weight participants. The percentage of people with the Pro12Ala mutation was not signi®cantly different in obese or normal weight participants (20% and 15%, respectively; P 0.32). Conversely, in obese participants with obesity starting in early adulthood (ie with BMI at age 25 above 26.9 kgam 2 which represents the median of the whole obese group), the Pro12Ala mutation was observed signi®cantly more frequently than in the normal weight controls (29% vs 15%; chi square 4.5, P`0.05; odds ratio 2.4; 95% CI 1.03 ± 5.36). No association of the Pro12Ala variant with any of the component of the metabolic syndrome measured in the study was observed in either obese, juvenile obese or normal weight participants. CONCLUSIONS: Results of this study indicate that the Pro12Ala mutation does not play a major role as a determinant of severe obesity andaor features of the metabolic syndrome in the general population. However, this mutation may be of greater importance as a contributor to early onset obesity.