title: Evaluation of HOMA and QUICKI as measures of insulin sensitivity in prepubertal children.
abstract: BACKGROUND
  Simple fasting sample methods to measure insulin sensitivity (SI) 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 SI in prepubertal children.
  
  
  METHODS
  The study population consisted of twins (n = 44), premature (n = 17), small for gestational age (SGA) (15), and normal (n = 3) prepubertal children. The insulin-sensitivity index derived by the minimal model (SIMM) 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 (RHOMA) and QUICKI were calculated from fasting plasma glucose and insulin values.
  
  
  RESULTS
  The correlation between RHOMA and SIMM (r = -0.4, p < 0.001) was no better than that between fasting insulin and SIMM (r = -0.4, p < 0.001). QUICKI was poorly correlated with SIMM (r = 0.2, p = 0.02). The correlation between SIMM and RHOMA is largely confined to low SI values (< 10 x 10(-4)/min microU/mL.) In seven SGA subjects, the introduction of growth hormone treatment led to an expected fall in SIMM by 8.2 +/- 2.8 x 10(-4)/min microU/mL (p = 0.02) that was not detected by either RHOMA (p = 0.1) or QUICKI (p = 0.2). Similarly, SIMM values were lower in obese (n = 9) compared to non-obese subjects (p = 0.04); however, no difference was found between these two groups with either RHOMA (p = 0.21) or QUICKI (p = 0.8).
  
  
  CONCLUSIONS
  As measures of SI in prepubertal children, RHOMA is no better than fasting insulin and QUICKI, a poor measure. Neither RHOMA nor QUICKI was able to detect changes in SI induced by either obesity or growth hormone therapy.
authors.affiliation: Department of Paediatrics and the Health Research Council Biostatistics Unit, University of Auckland, Private Bag 92019, Auckland, New Zealand. w.cutfield@auckland.ac.nz
authors.forename: Wayne S
authors.initials: WS
authors.lastname: Cutfield
authors.forename: Craig A
authors.initials: CA
authors.lastname: Jefferies
authors.forename: Wendy E
authors.initials: WE
authors.lastname: Jackson
authors.forename: Elizabeth M
authors.initials: EM
authors.lastname: Robinson
authors.forename: Paul L
authors.initials: PL
authors.lastname: Hofman
mesh_terms: D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D002648:Child; D004784:Environmental Monitoring / Q000379:methods*; D005215:Fasting; D005260:Female; D005317:Fetal Growth Retardation / Q000097:blood*; D006706:Homeostasis; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000097:blood; D007236:Infant, Small for Gestational Age / Q000097:blood; D007328:Insulin / Q000097:blood* / Q000494:pharmacology; D008297:Male; D008954:Models, Biological; D011627:Puberty; D012016:Reference Values; D015203:Reproducibility of Results
chemical_list: D001786:Blood Glucose; D007328:Insulin