Original Article Evaluation of HOMA and QUICKI as measures of insulin sensitivity in prepubertal children Cutfield WS, Jefferies CA, Jackson WE, Robinson EM, Hofman PL. Evaluation of HOMA and QUICKI as measures of insulin sensitivity in prepubertal children. Pediatric Diabetes 2003: 4: 119—125. # Blackwell Munksgaard, 2003. Abstract: Background: Simple fasting sample methods to measure insulin sensitivity (S I ) such as homeostasis model assessment (HOMA) and quantitative insulin-sensitivity check index (QUICKI) have been widely promoted in adult studies but have not been formally evaluated in children. The aim of this study was to compare HOMA and QUICKI to the minimal model as measures of S I in prepubertal children. Method: The study population consisted of twins (n ¼ 44), premature (n ¼ 17), small for gestational age (SGA) (15), and normal (n ¼ 3) prepubertal children. The insulin-sensitivity index derived by the minimal model (S I MM ) was calculated by the minimal model with plasma glucose and insulin data from a 90-min frequently sampled intravenous glucose test with tolbutamide. The HOMA resistance index (R HOMA ) and QUICKI were calculated from fasting plasma glucose and insulin values. Results: The correlation between R HOMA and S IMM (r ¼0.4, p < 0.001) was no better than that between fasting insulin and S I MM (r ¼0.4, p < 0.001). QUICKI was poorly correlated with S IMM (r ¼ 0.2, p ¼ 0.02). The correlation between S I MM and R HOMA is largely confined to low S I values (<10  10 4 /min mU/mL). In seven SGA subjects, the introduction of growth hormone treatment led to an expected fall in S IMM by 8.2  2.8  10 4 /min mU/mL (p ¼ 0.02) that was not detected by either R HOMA (p ¼ 0.1) or QUICKI (p ¼ 0.2). Similarly, S I MM values were lower in obese (n ¼ 9) compared to non-obese subjects (p ¼ 0.04); however, no difference was found between these two groups with either R HOMA (p ¼ 0.21) or QUICKI (p ¼ 0.8). Conclusion: As measures of S I in prepubertal children, R HOMA is no better than fasting insulin and QUICKI, a poor measure. Neither R HOMA nor QUICKI was able to detect changes in S I induced by either obesity or growth hormone therapy. Wayne S. Cutfield a , Craig A. Jefferies a , Wendy E. Jackson a , Elizabeth M. Robinson b and Paul L. Hofman a a Department of Paediatrics and the Health Research Council Biostatistics Unit; and b Department of Community Health, University of Auckland, Auckland, New Zealand Key words: HOMA — insulin sensitivity — minimal model — prepubertal children — QUICKI Corresponding author: Dr Wayne Cutfield, Liggins Institute, Faculty of Medicine and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand. Tel: þ64-9-3737-599x84476; fax: þ64-9-3074-913; e-mail: w.cutfield@auckland.ac.nz Submitted 30 January 2003. Accepted for publication 16 May 2003 Insulin is a critical component in glucose homeostasis. The development of an insulin radioimmunoassay in the 1950s was an important early step toward the later development of techniques to estimate insulin-mediated glucose uptake (1). A reduction in insulin sensitivity (S I ) (insulin resistance) has been shown to be an early defect in the development of type 2 diabetes mellitus (2, 3). Furthermore, reduced S I and compensatory hyperinsulinism are involved in the pathophysiology of obesity, hypertension, and dyslipidemias (4, 5). To date, the majority of S I studies have focussed on under- standing the sequence of events that lead to the development of type 2 diabetes mellitus in adults. Over the past 15yr, a variety of methods have been developed to measure S I . These methods can be clus- tered into two groups: complex, invasive, and precise methods such as the euglycemic clamp and modified minimal model; and simple methods based upon fasting Pediatric Diabetes 2003: 4: 119—125 Copyright # Blackwell Munksgaard 2003 Printed in Denmark. All rights reserved Pediatric Diabetes ISSN 1399-543X 119