Metabolism - Clinical and Experimental
Volume 46, Issue 4 , Pages 395-399, April 1997

The insertion allele at the angiotensin I—Converting enzyme gene locus is associated with insulin resistance☆☆☆

  • Ken C. Chiu

      Affiliations

    • Corresponding Author InformationAddress reprint requests to Ken C. Chiu, MD, Division of Endocrinology and Metabolism, UCLA School of Medicine, 10833 Le Conte Ave, 46-118CHS, Los Angeles, CA 90095-1682.
    • ,
  • Jennifer E. McCarthy

Division of Endocrinology and Metabolism, University of California, Los Angeles, School of Medicine, Los Angeles, CA, USA

Received 24 June 1996; accepted 14 November 1996.

Abstract 

Plasma angiotensin I—converting enzyme (ACE) levels are genetically predetermined and are correlated with a deletion (D) insertion (I) polymorphism at the ACE gene locus. A subset of diabetic patients are noted to have elevated ACE levels. Treatment with ACE inhibitors has been shown to improve insulin sensitivity in both diabetic and nondiabetic subjects. We examined the relationship of polymorphism and insulin sensitivity in 24 glucose-tolerant subjects by an oral glucose tolerance test (OGTT) and glucose clamps. Subjects with the I allele had higher insulin levels at 90 minutes (515 ± 69 v 250 ± 43 pmol/L, P = .008) and higher insulin area under the curve (56,200 ± 8,148 v 33,300 ± 8,114, P = .022) after glucose challenge compared with subjects without the I allele. During the euglycemic clamp, subjects with the I allele require less glucose infusion to maintain euglycemia than subjects without the I allele (5.343 ± 0.743 v 8.944 ± 1.272 mg/kg/min, P = .020). We conclude that the I allele is associated with insulin resistance in glucose-tolerant and normotensive African-Americans.

No full text is available. To read the body of this article, please view the PDF online.

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

☆ Supported in part by gifts from the Oberkotter Foundation and Children's Diabetes Foundation, and a grant from the American Diabetes Association, Grant No. DK20579-11 (Diabetes Research and Training Center, Washington University School of Medicine) from the National Institute of Diabetes and Digestive and Kidney Diseases, and Grant No. MO1RR00036 (General Clinical Research Center, Washington University School of Medicine) from the National Institutes of Health.

☆☆ Presented in abstract form at the 56th Annual Scientific Meetings and Sessions, American Diabetes Association, San Francisco, CA, June 8–11, 1996.

PII: S0026-0495(97)90054-8

Metabolism - Clinical and Experimental
Volume 46, Issue 4 , Pages 395-399, April 1997

Article Tools