Access to the PDF text

Free Article !

Diabetes & Metabolism
Volume 36, n° 3
pages 247-249 (juin 2010)
Doi : 10.1016/j.diabet.2010.01.006
Received : 31 December 2009 ;  accepted : 5 January 2010
Reproducibility of HOMA and QUICKI among individuals with variable glucose tolerance
Reproductibilité des indices HOMA et QUICKI entre individus avec une tolérance variable au glucose

A. Borai a, , C. Livingstone a, b, A. Farzal c, M. Kholeif c, T. Wang b, G. Ferns a, b
a Faculty of Health and Medical Sciences, University of Surrey, Stag Hill, Guildford, Surrey, GU2 7XH, UK 
b Department of Clinical Biochemistry, Royal Surrey County Hospital, Egerton Road, Guildford, Surrey, GU2 7XX, UK 
c Department of Pathology, King Abdulaziz Medical City, PO Box 9515, Jeddah 21423, Saudi Arabia 

Corresponding author.

Keywords : HOMA-β, HOMA-IR, QUICKI, Reproducibility, Insulin resistance

Mots clés : HOMA-β, HOMA-IR, QUICKI, Reproductibilité, Résistance à l’insuline

To the editor,

We read with interest the article published in this journal by Antuna-Puente et al. [1]. The authors are to be complimented on their efforts to study the reproducibility of the formulae of two key indices of insulin resistance – namely, homoeostasis model assessment (HOMA) and the quantitative insulin-sensitivity check index (QUICKI). Their conclusion that coefficients of variation (CVs) should be applied to assess the reproducibility of techniques to measure glucose and insulin rather than of mathematical formulae is an important one, and we agree with their conclusion that insulin variation is likely to be the main determinant of variations in these simple indices of insulin resistance. Whilst the authors have reported absolute CV values for non-diabetic subjects, we have taken this a step further by investigating the trend of these CVs in subjects with different degrees of glucose tolerance. Our findings may have a potential impact on future studies of simple indices of insulin resistance and their clinical application.

We used insulin and glucose data obtained from a previous study of biological variations of insulin-like growth factor-binding protein-1 (IGFBP-1) [2]. The CVs for the HOMA of β-cell function (HOMA-β; 20×fasting insulin (mU/L)/[fasting glucose (mmol/L)3.5] and of insulin resistance (HOMA-IR; fasting glucose (mmol/L)×fasting insulin (mU/L)/22.5), and for QUICKI (1/[log insulin (μU/mL)+log glucose (mg/dL)]) [3, 4], were investigated in subjects from all glucose-tolerance categories. The CVs were obtained over two consecutive visits.

Subjects were between 20 and 65 years of age, with a body mass index (BMI) >20 and <35kg/m2. Each subject attended the clinic on two occasions, separated by an average interval of 10 days. For both visits, subjects fasted for 10h prior to blood sampling. The glycaemic status of each individual was determined by a standard 75-g oral glucose tolerance test (OGTT) on the first visit, with subjects classified according to WHO criteria [5]. A further fasting sample was collected during the second visit while investigating frequently sampled intravenous glucose tolerance (FSIVGTT) for another study [6]. All patients with type 2 diabetes (DM) were being treated by dietary means alone and had not previously received either oral antidiabetic medications or insulin, and none was being treated with steroids or thyroxine. Participants were instructed to avoid modifying their lifestyles, or exercise and eating patterns, from one week prior to the first blood test until completion of the study. The study was approved by the King Abdulaziz Medical City (Jeddah, Kingdom of Saudi Arabia) and the South West Surrey Local Research Ethics Committee (LREC) at the Royal Surrey County Hospital, Guildford, UK. Informed written consent was obtained from all subjects prior to participation. Within-individual CVs were calculated using the modified method for paired samples between the two visits [7].

Categorization of the subjects was as follows: normal glucose tolerance (NGT=15); impaired fasting glucose (IFG=9); impaired glucose tolerance (IGT=9); and DM=9. The means and CVs of HOMA-β, HOMA-IR and QUICKI are presented in Table 1. As shown in Fig. 1, the %CV for the HOMA-β model was 17.4% in the NGT subjects and increased with deteriorating glucose tolerance, reaching 68.7% in DM patients. The %CV for HOMA-IR in the NGT group was 25.7%, which reached 52.1% in the DM group. QUICKI showed the greatest reproducibility, with a maximum %CV of 5.8% in DM patients.

Fig. 1

Fig. 1. 

Trends of reproducibility for HOMA-β, HOMA-IR and QUICKI in subjects with various degrees of glucose tolerance. NGT: normal glucose tolerance; IFG: impaired fasting glucose; IGT: impaired glucose tolerance.


Our outcomes for HOMA-IR and QUICKI were comparable to those of Antuna-Puente et al., [1], which involved non-diabetic subjects, although the CVs for the same indices were lower in NGT subjects compared with the other glycaemia categories. However, this was most probably due to the variable activity of β-cell function in DM compared with NGT individuals (Table 1).

In those with DM, Emoto et al. [8] and Sarafidis et al. [9] both reported lower CVs for HOMA-IR (11.7% and 23.5%, respectively) compared with Jayagopal et al. [10] and the CVs obtained in our study (79.3% and 52.1%, respectively). This might be explained by the presence of insulin-resistance-modifying medications, resulting in an improved reproducibility of the measured index. In contrast, in both Jayagopal et al. and our present study, patients with DM were not discontinued or receiving any insulin-resistance-modifying medications that might have caused the reproducibility of indices to deteriorate progressively with increasing severity of glucose intolerance.

In conclusion, it is important for those carrying out epidemiological studies to be aware of the observation that trends of biological variations of simple indices of insulin resistance, in addition to those of insulin levels, are greatly influenced by the degree of glucose tolerance and by insulin-resistance-modifying medications. These factors would also be expected to affect the reproducibility not only of HOMA-IR and QUICKI, but of all other indices of insulin resistance as well.

Conflicts of interest

The authors do not have any conflicts of interest to declare.


The authors gratefully acknowledge the financial support of the Kingdom of Saudi Arabia government, as represented by the Saudi National Guard Health Affairs.


Antuna-Puente B., Faraj M., Karelis A.D., Garrel D., Prud’homme D., Rabasa-Lhoret R., and al. HOMA or QUICKI: Is it useful to test the reproducibility of formulas? Diabetes Metab 2008 ;  34 : 294-296 [inter-ref]
Borai A., Livingstone C., Mehta S., Zarif H., Abdelaal F., Ferns G. Biological variation in fasting serum insulin-like growth factor binding protein-1 (IGFBP-1) among individuals with a varying glucose tolerance Clin Biochem 2009 ;  42 : 1270-1274 [cross-ref]
Matthews D.R., Hosker J.P., Rudenski A.S., Naylor B.A., Treacher D.F., Turner R.C. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man Diabetologia 1985 ;  28 : 412-419 [cross-ref]
Katz A., Nambi S.S., Mather K., Baron A.D., Follmann D.A., Sullivan G., and al. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans J Clin Endocrinol Metab 2000 ;  85 : 2402-2410 [cross-ref]
Alberti K.G., Zimmet P.Z. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation Diabet Med 1998 ;  15 : 539-553 [cross-ref]
Borai A, Callum L, Hawazen Z, Shweta M, Mona K, Mohammed A, et al. A comparative study of insulin resistance for Saudi and Caucasian subjects across a range of glycaemic categories. Diabetes and metabolic syndrome: Clinical research and reviews. 2009; 3:204–10.
Raggatt P.R. Duplicates or singletons? An analysis of the need for replication in immunoassay and a computer program to calculate the distribution of outliers, error rate and the precision profile from assay duplicates Ann Clin Biochem 1989 ;  26 (Pt 1) : 26-37
Emoto M., Nishizawa Y., Maekawa K., Hiura Y., Kanda H., Kawagishi T., and al. Homeostasis model assessment as a clinical index of insulin resistance in type 2 diabetic patients treated with sulfonylureas Diabetes Care 1999 ;  22 : 818-822 [cross-ref]
Sarafidis P.A., Lasaridis A.N., Nilsson P.M., Pikilidou M.I., Stafilas P.C., Kanaki A., and al. Validity and reproducibility of HOMA-IR, 1/HOMA-IR, QUICKI and McAuley’s indices in patients with hypertension and type II diabetes J Hum Hypertens 2007 ;  21 : 709-716 [cross-ref]
Jayagopal V., Kilpatrick E.S., Jennings P.E., Hepburn D.A., Atkin S.L. Biological variation of homeostasis model assessment-derived insulin resistance in type 2 diabetes Diabetes Care 2002 ;  25 : 2022-2025 [cross-ref]

© 2010  Published by Elsevier Masson SAS.
EM-CONSULTE.COM is registrered at the CNIL, déclaration n° 1286925.
As per the Law relating to information storage and personal integrity, you have the right to oppose (art 26 of that law), access (art 34 of that law) and rectify (art 36 of that law) your personal data. You may thus request that your data, should it be inaccurate, incomplete, unclear, outdated, not be used or stored, be corrected, clarified, updated or deleted.
Personal information regarding our website's visitors, including their identity, is confidential.
The owners of this website hereby guarantee to respect the legal confidentiality conditions, applicable in France, and not to disclose this data to third parties.
Article Outline
You can move this window by clicking on the headline