Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Cytokine. 2008 Oct;44(1):201-6. doi: 10.1016/j.cyto.2008.08.001. Epub 2008 Sep 11.

Genetic variants in STAT3 are associated with nonalcoholic fatty liver disease.

Author information

  • 1Department of Molecular Genetics and Biology of Complex Diseases, Institute of Medical Research A. Lanari, University of Buenos Aires-CONICET, Ciudad Autónoma de Buenos Aires, Argentina. ssookoian@lanari.fmed.uba.ar

Abstract

AIMS:

To investigate the role of gene variants and derived haplotypes of the STAT3 transcription factor in nonalcoholic fatty liver disease (NAFLD) and their relation with the clinical disease severity.

PATIENTS AND METHODS:

108 patients with NAFLD and different stages of clinical disease severity, and a group of 55 healthy individuals were included in a Hospital-based study. We selected 3 tagSNPs showing a minor allele frequency >10% (rs2293152 C/G, rs6503695 C/T, and rs9891119 A/C) encompassing 68.55kb in chromosome 17, representing 24 polymorphic sites (r(2)>0.8).

RESULTS:

In univariate analysis, there were significant differences in the allele frequency of the rs6503695 and rs9891119 between the healthy individuals and NAFLD patients (empiric P=0.021 and 0.020, respectively). The test results for the multi-marker analysis showed that haplotypes TA and CC of tagSNPs rs6503695, rs9891119 were significantly associated with NAFLD (empiric P=0.035 and 0.015, respectively). When we tested the hypothesis of a relation between the gene variants and the clinical and histological spectrum of NAFLD by multinomial analysis, a significant association was observed with rs9891119 (P=0.02).

CONCLUSIONS:

Our study suggests a potential role of the STAT3 polymorphisms and their haplotypes in susceptibility to NAFLD and disease severity.

PMID:
18789715
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk