Apolipoprotein A5 T-1131C Variant Confers Risk for Metabolic Syndrome

Anita MAÁSZ1, Péter KISFALI1, Katalin HORVATOVICH1, Márton MOHÁS2, Lajos MARKÓ2, Veronika CSÖNGEI1, Bernadett FARAGÓ1, Luca JÁROMI1, Lili MAGYARI1, Enikõ SÁFRÁNY1, Csilla SIPEKY1, István WITTMANN2, Béla MELEGH1

1Department of Medical Genetics and Child Development, University of Pécs, Pécs, Hungary
22nd Department of Medicine and Nephrological Center, University of Pécs, Pécs, Hungary


The -1131C is a naturally occurring variant of the apolipoprotein A5 (ApoA5) gene, which has been shown to associate with increased triglyceride levels. This variant has also been shown to confer risk for development of ischemic heart disease and stroke. The gene is in linkage disequilibrium with factors known to correlate with impaired glucose homeostasis. These observations prompted us to study the prevalence of the ApoA5 -1131C allele in patients with metabolic syndrome. A total of 201 metabolic syndrome patients and 210 controls were studied. In both groups the triglyceride levels of patients with -1131C allele were significantly increased compared to the subjects with -1131T allele (3.22+/-0.43 mmol/l vs. 2.24+/-0.12 mmol/l, p<0.01 in the metabolic syndrome patients; 2.10+/-0.19 mmol/l vs. 1.22+/-0.05 mmol/l, p<0.01 in the controls). In metabolic syndrome patients the prevalence of the ApoA5 -1131C variant was increased compared to the healthy controls (11% vs. 6.20%). Multiplex regression analysis model adjusted for age, gender, serum total cholesterol levels, acute myocardial infarction and stroke events revealed that the examined ApoA5 variant confers risk for the development of metabolic syndrome: the odds ratio at 95% confidence interval was 3.622 (1.200-10.936), p=0.02. Our findings strongly suggest that this variant is a risk factor for the development of hypertriglyceridemia and metabolic syndrome. Pathology & Oncology Research, Vol 13, Nr 3, 243-247, 2007

Key words: metabolic syndrome; glucose intolerance; ApoA5; T-1131C

Received: Dec 5, 2006; accepted: Aug 10, 2007
Correspondence: Béla MELEGH, Department of Medical Genetics and Child Development, University of Pécs, Szigeti 12 Pécs H-7624, Hungary; Tel: 00-36-72-536-427, Fax: 00-36-72-536-427; E-mail:

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