Preanalytical, Analytical, and Computational Factors Affect Homeostasis Model Assessment Estimates
- Susan E. Manley, PHD, FRCPATH12,
- Stephen D. Luzio, PHD, FRCPATH3,
- Irene M. Stratton, MSC4,
- Tara M. Wallace, MD, MRCP5 and
- Penelope M.S. Clark, PHD, FRCPATH26
- 1Clinical Biochemistry, University Hospital Birmingham NHS Foundation Trust, University of Birmingham, Birmingham, U.K.
- 2Division of Medical Sciences, University of Birmingham, Birmingham, U.K.
- 3Diabetes Research Unit, Cardiff University, Cardiff, U.K.
- 4English National Diabetic Retinopathy Screening Programme, Gloucestershire Hospitals NHS Foundation Trust, Cheltenham, U.K.
- 5Norfolk and Norwich University Hospital, Norwich, U.K.
- 6The Regional Endocrine Laboratory, University Hospital Birmingham NHS Foundation Trust, University of Birmingham, Birmingham, U.K.
- Corresponding author: Dr. Sue Manley, susan.manley{at}uhb.nhs.uk
Abstract
OBJECTIVE—We investigated how β-cell function and insulin sensitivity or resistance are affected by the type of blood sample collected or choice of insulin assay and homeostatis model assessment (HOMA) calculator (http://www.dtu.ox.ac.uk).
RESEARCH DESIGN AND METHODS—Insulin was measured using 11 different assays in serum and 1 assay in heparinized plasma. Fasting subjects with normoglycemia (n = 12), pre-diabetes, i.e., impaired fasting glucose or impaired glucose tolerance (n = 18), or type 2 diabetes (n = 67) were recruited. Patients treated with insulin or those who were insulin antibody–positive were excluded. HOMA estimates were calculated using specific insulin (SI) or radioimmunoassay (RIA) calculators (version 2.2).
RESULTS—All glucose values were within model (HOMA) limits but not all insulin results, as 4.3% were <20 pmol/l and 1% were >300 pmol/l. β-Cell function derived from different insulin assays ranged from 67 to 122% (median) for those with normoglycemia (P = 0.026), from 89 to 138% for those with pre-diabetes (P = 0.990), and from 50 to 81% for those with type 2 diabetes (P < 0.0001). Furthermore, insulin resistance ranged from 0.8 to 2.0 (P = 0.0007), from 1.9 to 3.2 (P = 0.842), and from 1.5 to 2.9 (P < 0.0001), respectively. This twofold variation in HOMA estimates from the various insulin assays studied in serum may be significant metabolically. Insulin was 15% lower in heparinized plasma (used in the original HOMA study) compared with serum, which is now more commonly used. β-Cell function differed by 11% and insulin resistance by 15% when estimates derived from specific insulin were calculated using the RIA rather than the SI calculator.
CONCLUSIONS—To enable comparison of HOMA estimates among individuals and different research studies, preanalytical factors and calculator selection should be standardized with insulin assays traceable to an insulin reference method procedure.
Footnotes
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Published ahead of print at http://care.diabetesjournals.org on 5 June 2008.
S.E.M. and S.D.L. contributed equally to this study.
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- Accepted May 28, 2008.
- Received January 15, 2008.
- DIABETES CARE
