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Indexes of Insulin Resistance and Secretion in Obese Children and Adolescents

A validation study

¹ Department of Endocrinology and Diabetes, Royal Children’s Hospital, Herston, Brisbane, Queensland, Australia
² Department of Kinesiology and Community Health Institute, Kansas State University, Manhattan, Kansas
³ School of Human Movement Studies, University of Queensland, St. Lucia, Brisbane, Queensland, Australia

Address correspondence and reprint requests to Louise S. Conwell, MBBS, FRACP, Royal Children’s Hospital Foundation Clinical Research Fellow, Department of Endocrinology and Diabetes, Royal Children’s Hospital, Herston, Brisbane, Queensland, Australia, 4029. E-mail: louise_conwell{at}health.qld.gov.au

OBJECTIVE—To assess the concurrent validity of fasting indexes of insulin sensitivity and secretion in obese prepubertal (Tanner stage 1) children and pubertal (Tanner stages 2–5) adolescents using estimates from the modified minimal model frequently sampled intravenous glucose tolerance test (FSIVGTT) as a criterion measure.

RESEARCH DESIGN AND METHODS—Eighteen obese children and adolescents (11 girls and 7 boys, mean age 12.2 ± 2.4 years, mean BMI 35.4 ± 6.2 kg/m², mean BMI-SDS 3.5 ± 0.5, 7 prepubertal and 11 pubertal) participated in the study. All participants underwent an insulin-modified FSIVGTT on two occasions, and 15 repeated this test a third time (mean 12.9 and 12.0 weeks apart). S_i measured by the FSIVGTT was compared with homeostasis model assessment (HOMA) of insulin resistance (HOMA-IR), quantitative insulin-sensitivity check index (QUICKI), fasting glucose-to-insulin ratio (FGIR), and fasting insulin (estimates of insulin sensitivity derived from fasting samples). The acute insulin response (AIR) measured by the FSIVGTT was compared with HOMA of percent ß-cell function (HOMA-ß%), FGIR, and fasting insulin (estimates of insulin secretion derived from fasting samples).

RESULTS—There was a significant negative correlation between HOMA-IR and S_i (r = -0.89, r = -0.90, and r = -0.81, P < 0.01) and a significant positive correlation between QUICKI and S_i (r = 0.89, r = 0.90, and r = 0.81, P < 0.01) at each time point. There was a significant positive correlation between FGIR and S_i (r = 0.91, r = 0.91, and r = 0.82, P < 0.01) and a significant negative correlation between fasting insulin and S_i (r = -90, r = -0.90, and r = -0.88, P < 0.01). HOMA-ß% was not as strongly correlated with AIR (r = 0.60, r = 0.54, and r = 0.61, P < 0.05).

CONCLUSIONS—HOMA-IR, QUICKI, FGIR, and fasting insulin correlate strongly with S_i assessed by the FSIVGTT in obese children and adolescents. Correlations between HOMA-ß%, FGIR and fasting insulin, and AIR were not as strong. Indexes derived from fasting samples are a valid tool for assessing insulin sensitivity in prepubertal and pubertal obese children.

Abbreviations: AIR, acute insulin response • FGIR, fasting glucose-to-insulin ratio • FSIVGTT, frequently sampled intravenous glucose tolerance test • HOMA, homeostasis model assessment • HOMA-ß%, HOMA of percent ß-cell function • HOMA-IR, HOMA of insulin resistance • QUICKI, quantitative insulin-sensitivity check index

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