Biological Variation of Homeostasis Model Assessment-Derived Insulin Resistance in Type 2 Diabetes

  1. Vijay Jayagopal, MRCP1,
  2. Eric S. Kilpatrick, MRCPATH2,
  3. Paul E. Jennings, FRCP13,
  4. David A. Hepburn, FRCP1 and
  5. Stephen L. Atkin, FRCP1
  1. 1Department of Medicine, University of Hull, Hull, U.K
  2. 2Department of Clinical Biochemistry, Hull Royal Infirmary, Hull, U.K
  3. 3Department of Medicine, York District General Hospital, York, U.K

    Abstract

    OBJECTIVE—Individuals with type 2 diabetes are particularly vulnerable to cardiovascular disease. Insulin resistance is a major determinant of this increased risk and is a potential therapeutic target. This study was undertaken to establish the natural biological variation of insulin resistance in individuals with type 2 diabetes.

    RESEARCH DESIGN AND METHODS—The biological variation of insulin resistance was assessed by measuring insulin resistance at 4-day intervals on 10 consecutive occasions in 12 postmenopausal women with diet-controlled type 2 diabetes and in 11 weight- and age-matched postmenopausal women without type 2 diabetes. Insulin resistance was derived using the homeostasis model assessment for insulin resistance (HOMA-IR) method.

    RESULTS—The distribution of HOMA-IR was log Gaussian in the type 2 diabetic study group and Gaussian in the control group. The HOMA-IR in the type 2 diabetic group was significantly greater than that of the control group (mean ± SD: 4.33 ± 2.3 vs. 2.11 ± 0.79 units, P = 0.001). After accounting for analytical variation, the mean intraindividual variation was also substantially greater in the type 2 diabetic group than in the control group (mean 1.05 vs. 0.15, P = 0.001). Consequently, at any level of HOMA-IR, a subsequent sample must increase by >90% or decrease by >47% to be considered significantly different from the first.

    CONCLUSIONS—HOMA-IR is significantly greater and more variable for individuals with type 2 diabetes. Therefore, this inherent variability needs to be accounted for in studies evaluating therapeutic reduction of HOMA-IR in this group.

    Footnotes

    • Address correspondence and reprint requests to Dr. V. Jayagopal, Michael White Centre for Diabetes and Endocrinology, Brocklehurst Building, Hull Royal Infirmary, 220-236 Anlaby Rd., Hull, HU3 2RW, U.K. E-mail: v.jaygopal{at}hull.ac.uk.

      Received for publication 7 February 2002 and accepted in revised form 22 July 2002.

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