Summary
The peroxisome-proliferator-activated receptor γ2 (PPAR γ2) is a transcriptional key
regulator of adipocyte differentiation. PPARγ2 can be inactivated by phosphorylation
of a serine residue at position 114. A point mutation leading to an amino acid exchange
at position 115 (Pro115Gln) was shown to preclude serine phosphorylation and to consecutively
accelerate adipocyte differentiation emphasizing the pathophysiological relevance
of this mutation.
So far, four markedly obese heterozygote carriers of the Pro115Gln mutation (body
mass index 37.9-47.3 kg×m-2) have been identified in a circumscribed study population. In order to evaluate the
epidemiological relevance of the Pro115Gln mutation in morbid obesity we screened
the DNA of all subjects with a body mass index greater than 35 kg×m-2 who had participated in a nationwide German epidemiological field survey. There was
no homozygote or heterozygote carrier of the Pro115Gln polymorphism among them. We
conclude that the Pro115Gln polymorphism within the PPAR γ2 gene has no relevant epidemiological
impact on morbid obesity in Germany. It needs further investigation whether this polymorphism
might play a role in related metabolic disorders.
Key words:
Peroxisome-proliferator-activated receptor γ2 - Pro115Gln - Obesity - Polymorphism
- Epidemiology
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Dr. O. Hamer
Klinik und Poliklinik für Innere Medizin I
Universitätsklinik Regensburg
93042 Regensburg
Germany
Telefon: +49- 941-944 7001
Fax: +49- 941-944 7002
eMail: okka.hamer@klinik.uni-regensburg.de