Abstract

Background: Osteopontin (OPN)-transgenic mice exhibit increased carotid artery intima-media thickness (CIMT), smooth muscle cell proliferation, and atheroma formation. Methods: An association of the human T-66G promoter variant with CIMT was examined in Caucasian adults grouped according to metabolic syndrome criteria: present (+MetS; n = 70) or absent (-MetS; n = 70). Results: The G-allele frequency was 22%. For the entire cohort, the G group (TG and GG) was associated with significantly lower age-adjusted and gender-adjusted CIMT compared with the TT group (P = .008); similar analysis by metabolic syndrome group found a significant difference only in the -MetS group (P = .018). Stepwise multivariate regression showed that after age and waist circumference, the T-66G variant was the next most predictive of CIMT (P = .007). These data suggest that in a normoglycemic environment, human vascular OPN gene expression contributes to arterial structure, an effect diminished in dysmetabolic states. Conclusion: Humans with the OPN -66 TT genotype, particularly those without metabolic syndrome, exhibit thicker CIMT.

Original languageEnglish
Pages (from-to)954-960
Number of pages7
JournalJournal of the American Society of Echocardiography
Volume21
Issue number8
DOIs
StatePublished - Aug 2008

Keywords

  • Arteriosclerosis
  • Carotid arteries
  • Genetics
  • Growth substances
  • Metabolic syndrome

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