The Insertion Allele of the ACE Gene I/D Polymorphism

DOI Web Site 2 Citations
  • Arshia Panahloo
    From the Departments of Medicine (A.P., C.A., V.M.-A., J.S.Y.) and Primary Health Care (M.M.G.), University College London Medical School, Whittington Hospital, Archway Road, London, and Division of Cardiovascular Genetics (P.T., S.E.H.), Department of Medicine, University College London Medical School, Rayne Institute, University Street, London, England.
  • Christine Andrès
    From the Departments of Medicine (A.P., C.A., V.M.-A., J.S.Y.) and Primary Health Care (M.M.G.), University College London Medical School, Whittington Hospital, Archway Road, London, and Division of Cardiovascular Genetics (P.T., S.E.H.), Department of Medicine, University College London Medical School, Rayne Institute, University Street, London, England.
  • Vidya Mohamed-Ali
    From the Departments of Medicine (A.P., C.A., V.M.-A., J.S.Y.) and Primary Health Care (M.M.G.), University College London Medical School, Whittington Hospital, Archway Road, London, and Division of Cardiovascular Genetics (P.T., S.E.H.), Department of Medicine, University College London Medical School, Rayne Institute, University Street, London, England.
  • Mairi M. Gould
    From the Departments of Medicine (A.P., C.A., V.M.-A., J.S.Y.) and Primary Health Care (M.M.G.), University College London Medical School, Whittington Hospital, Archway Road, London, and Division of Cardiovascular Genetics (P.T., S.E.H.), Department of Medicine, University College London Medical School, Rayne Institute, University Street, London, England.
  • Phillipa Talmud
    From the Departments of Medicine (A.P., C.A., V.M.-A., J.S.Y.) and Primary Health Care (M.M.G.), University College London Medical School, Whittington Hospital, Archway Road, London, and Division of Cardiovascular Genetics (P.T., S.E.H.), Department of Medicine, University College London Medical School, Rayne Institute, University Street, London, England.
  • Steve E. Humphries
    From the Departments of Medicine (A.P., C.A., V.M.-A., J.S.Y.) and Primary Health Care (M.M.G.), University College London Medical School, Whittington Hospital, Archway Road, London, and Division of Cardiovascular Genetics (P.T., S.E.H.), Department of Medicine, University College London Medical School, Rayne Institute, University Street, London, England.
  • John S. Yudkin
    From the Departments of Medicine (A.P., C.A., V.M.-A., J.S.Y.) and Primary Health Care (M.M.G.), University College London Medical School, Whittington Hospital, Archway Road, London, and Division of Cardiovascular Genetics (P.T., S.E.H.), Department of Medicine, University College London Medical School, Rayne Institute, University Street, London, England.

Bibliographic Information

Other Title
  • A Candidate Gene for Insulin Resistance?
Published
1995-12-15
DOI
  • 10.1161/01.cir.92.12.3390
Publisher
Ovid Technologies (Wolters Kluwer Health)

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Description

<jats:p> <jats:italic>Background</jats:italic> The insertion/deletion (ID) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with increased coronary heart disease (CHD), although the mechanism of this association is not apparent. We tested the hypothesis that the deletion allele of the ACE gene is associated with insulin resistance. </jats:p> <jats:p> <jats:italic>Methods and Results</jats:italic> We related ACE genotype to components of the insulin-resistance syndrome in 103 non–insulin-dependent diabetic (NIDDM) and 533 nondiabetic white subjects. NIDDM subjects with the DD genotype had significantly lower levels of specific insulin (DD 38.6, ID 57.1, and II 87.4 pmol · L <jats:sup>−1</jats:sup> by ANOVA, <jats:italic>P</jats:italic> =.011). Non–insulin-treated subjects with the DD genotype had increased insulin sensitivity by HOMA % (DD 56.4%, II 29.4%, <jats:italic>P</jats:italic> =.027) and lower levels of des 31,32 proinsulin (DD 3.3, II 7.6 pmol · L <jats:sup>−1</jats:sup> , <jats:italic>P</jats:italic> =.012) compared with II subjects. There were no differences in prevalence of CHD or levels of blood pressure, serum lipids, or plasminogen activator inhibitor–1 (PAI-1) activity between the three ACE genotypes. In nondiabetic subjects there were no differences in insulin sensitivity, levels of insulin-like molecules, blood pressure, PAI-1, serum lipids, or CHD prevalence between the three ACE genotypes. </jats:p> <jats:p> <jats:italic>Conclusions</jats:italic> We conclude that increased cardiovascular risk of the DD genotype is not mediated through insulin resistance or abnormalities in fibrinolysis. Conversely, we report an increased sensitivity in NIDDM subjects with the ACE DD genotype. </jats:p>

Journal

  • Circulation

    Circulation 92 (12), 3390-3393, 1995-12-15

    Ovid Technologies (Wolters Kluwer Health)

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