Endothelial Function Varies According to Insulin Resistance Disease Type

  1. Joshua A. Beckman, MD1,
  2. Allison B. Goldfine, MD1,
  3. Andrea Dunaif, MD1,
  4. Marie Gerhard-Herman, MD1 and
  5. Mark A. Creager, MD1
  1. From the 1Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts; the 2Division of Cellular and Molecular Physiology, Joslin Diabetes Center, Boston, Massachusetts; and the 3Division of Endocrinology, Northwestern University, Chicago, Illinois
  1. Address correspondence and reprint requests to Joshua A. Beckman, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St., Boston, MA 02115. E-mail: jbeckman{at}partners.org

Abstract

OBJECTIVE—We examined the relationship between insulin resistance and vascular function in three insulin-resistant states (type 2 diabetes, non-HIV lipodystrophic diabetes, and nondiabetic polycystic ovary syndrome [PCOS]) and in healthy control subjects.

RESEARCH DESIGN AND METHODS—The population included 12 women with type 2 diabetes, 6 with lipodystrophic diabetes, 10 with PCOS, and 19 healthy female subjects. Metabolic measures included insulin sensitivity by the homeostasis model assessment, lipids, free fatty acids, and adiponectin. High-resolution B-mode ultrasound was used to determine endothelium-dependent and -independent vasodilation.

RESULTS—Type 2 diabetic, liposdystrophic, and PCOS subjects were insulin resistant compared with control subjects (P = 0.001). Flow-mediated vasodilation was reduced in diabetic (3.4 ± 1.3%) compared with control (7.3 ± 1.1%) subjects but not in lipodystrophic (7.7 ± 1.2%) or PCOS (9.9 ± 0.7%) subjects (P = 0.005). Nitroglycerin-mediated vasodilation was attenuated in both diabetic (15.2 ± 2.0%) and lipodystrophic (16.7 ± 3.6%) subjects compared with healthy control (24.6 ± 2.4%) and PCOS (23.2 ± 1.8%) subjects (P = 0.019). Insulin resistance, free fatty acids, adiponectin, or C-reactive protein did not associate with vascular dysfunction.

CONCLUSIONS—Among these different types of patients with insulin resistance, we found abnormal endothelium-dependent vasodilation only in the patients with type 2 diabetes. We postulate that variations in the mechanism of insulin resistance may affect endothelial function differently than glucose homeostasis.

Footnotes

  • Published ahead of print at http://care.diabetesjournals.org on 29 January 2007. DOI: 10.2337/dc06-2142.

    A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C Section 1734 solely to indicate this fact.

    • Accepted January 21, 2007.
    • Received October 18, 2006.
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  1. Published online before print January 29, 2007, doi: 10.2337/dc06-2142 Diabetes Care May 2007 vol. 30 no. 5 1226-1232
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