Homeostatic model assessment

Short description: Method to quantify insulin resistance

The homeostatic model assessment (HOMA) is a method used to quantify insulin resistance and beta-cell function. It was first described under the name HOMA by Matthews et al. in 1985.

## Contents

* 1 Derivation
* 2 Notes
* 3 See also
* 4 References
* 5 External links

## Derivation

The HOMA authors used data from physiological studies to develop mathematical equations describing glucose regulation as a feedback loop.[1] They published computer software that solves the equations, so that insulin resistance and β-cell function can be estimated from fasting glucose and insulin levels. They also published an equation (see below) that gave approximately the same answers as an early version of the computer software.[2]

The computer model has since been improved to a HOMA2 model[3] to better reflect human physiology and recalibrated to modern insulin assays. In this updated version it is possible to determine insulin sensitivity and β-cell function from paired fasting plasma glucose and radioimmunoassay insulin, specific insulin, or C-peptide concentrations. The authors recommend the computer software be used wherever possible.[4][5]

## Notes

The HOMA model was originally designed as a special case of a more general structural (HOMA-CIGMA) model that includes the continuous infusion of glucose with model assessment (CIGMA) approach; both techniques use mathematical equations to describe the functioning of the major effector organs influencing glucose/insulin interactions.[6]

The approximating equation for insulin resistance, in the early model, used a fasting plasma sample, and was derived by use of the insulin-glucose product, divided by a constant: (assuming normal-weight, normal subjects < 35 years, having 100% β-cell function an insulin resistance of 1)

HOMA-IR=Glucose×Insulin22.5 | HOMA-IR=Glucose×Insulin405

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HOMA-β=20×InsulinGlucose−3.5% | HOMA-β=360×InsulinGlucose−63%
Glucose in Molar Units mmol/L | Glucose in mass units mg/dL

IR is insulin resistance and  %β  is the β-cell function (more precisely, an index for glucose tolerance, i.e. a measure for the ability to counteract the glucose load). Insulin is given in μU/mL.[7] Glucose and insulin are both during fasting.[2]

This model correlated well with estimates using the euglycemic clamp method (r = 0.88).[2]

The authors have tested HOMA and HOMA2 extensively against other measures of insulin resistance (or its reciprocal, insulin sensitivity) and β-cell function.[4] [8] [9]

The approximation formulae above relate to HOMA and are crude estimates of the model near normal levels of glucose and insulin in man. The actual calculated HOMA2 compartmental model is published [10] and is available online.

## See also

* QUICKI
* SPINA-GBeta
* SPINA-GR

## References

1. ↑ "Insulin deficiency and insulin resistance interaction in diabetes: estimation of their relative contribution by feedback analysis from basal plasma insulin and glucose concentrations.". Metabolism 28 (11): 1086–96. 1979. doi:10.1016/0026-0495(79)90146-X. PMID 386029.
2. ↑ 2.0 2.1 2.2 "Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.". Diabetologia 28 (7): 412–9. 1985. doi:10.1007/BF00280883. PMID 3899825.
3. ↑ A. S. Rudenski; D. R. Matthews; J. C. Levy; R. C. Turner (September 1991). "Understanding insulin resistance: Both glucose resistance and insulin resistance are required to model human diabetes". Metabolism 40 (9): 908–917. doi:10.1016/0026-0495(91)90065-5. ISSN 0026-0495. PMID 1895955.
4. ↑ 4.0 4.1 "Use and abuse of HOMA modeling.". Diabetes Care 27 (6): 1487–95. 2004. doi:10.2337/diacare.27.6.1487. PMID 15161807.
5. ↑ "Correct homeostasis model assessment (HOMA) evaluation uses the computer program.". Diabetes Care 21 (12): 2191–2. 1998. doi:10.2337/diacare.21.12.2191. PMID 9839117.
6. ↑ Turner et al. (1993) Measurement of insulin resistance and β-cell function: the HOMA and CIGMA approach. Current topics in diabetes research (eds) F. Belfiore, R. Bergman and G. Molinatti Front Diabetes. Basel, Karger 12: 66-75
7. ↑ "Surrogate markers of insulin resistance: A review". World J Diabetes 1 (2): 36–47. May 2010. doi:10.4239/wjd.v1.i2.36. PMID 21537426.
8. ↑ "Comparison of tests of beta-cell function across a range of glucose tolerance from normal to diabetes.". Diabetes 48 (9): 1779–86. 1999. doi:10.2337/diabetes.48.9.1779. PMID 10480608.
9. ↑ "Comparison of insulin sensitivity tests across a range of glucose tolerance from normal to diabetes.". Diabetologia 42 (6): 678–87. 1999. doi:10.1007/s001250051215. PMID 10382587.
10. ↑ "Expansion of the homeostasis model assessment of β-cell function and insulin resistance to enable clinical trial outcome modeling through the interactive adjustment of physiology and treatment effects: iHOMA2.". Diabetes Care 36 (8): 2324–30. 2013. doi:10.2337/dc12-0607. PMID 23564921.

## External links

* iHOMA - Nathan R Hill - University of Oxford
* iHOMA2 — Nuffield Department of Primary Care Health Sciences, University of Oxford

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Diabetes (E10–E14, 250)

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