Indexes of insulin resistance and secretion in obese children and adolescents a validation study

• Published in: Diabetes care Vol. 27; no. 2; pp. 314 - 319
• Main Authors: CONWELL, Louise S, TROST, Stewart G, BROWN, Wendy J, BATCH, Jennifer A
• Format: Journal Article
• Language: English
• Published: Alexandria, VA American Diabetes Association 01-02-2004
• Subjects: Adolescent; Biological and medical sciences; Blood Glucose - metabolism; Body Mass Index; Care and treatment; Child; Comparative analysis; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; European Continental Ancestry Group; Fasting; Female; Glucose Tolerance Test; Homeostasis; Humans; Insulin - blood; Insulin - metabolism; Insulin resistance; Insulin Resistance - physiology; Insulin Secretion; Islets of Langerhans - metabolism; Male; Medical sciences; Metabolic diseases; Models, Biological; Obesity; Obesity - blood; Obesity - physiopathology; Obesity in adolescence; Obesity in children; Puberty; Queensland; Reproducibility of Results; Type 2 diabetes; Queensland; Australia; Endocrinopathy; Human; Validation; Obesity; Secretion; Diabetes mellitus; Nutrition disorder; Index; Insulin; Target tissue resistance; Adolescent; Child; Nutritional status
• ISSN: 0149-5992; 1935-5548
• DOI: 10.2337/diacare.27.2.314

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.
Eighteen obese children and adolescents (11 girls and 7 boys, mean age 12.2 +/- 2.4 years, mean BMI 35.4 +/- 6.2 kg/m(2), 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 beta-cell function (HOMA-beta%), FGIR, and fasting insulin (estimates of insulin secretion derived from fasting samples).
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-beta% was not as strongly correlated with AIR (r = 0.60, r = 0.54, and r = 0.61, P < 0.05).
HOMA-IR, QUICKI, FGIR, and fasting insulin correlate strongly with S(i) assessed by the FSIVGTT in obese children and adolescents. Correlations between HOMA-beta%, 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.