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 Ϯ 2.4 years, mean BMI 35.4 Ϯ 6.2 kg/m 2 , mean BMI-SDS 3.5 Ϯ 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 ␤-cell function (HOMA-␤%), 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 ϭ Ϫ0.89, r ϭ Ϫ0.90, and r ϭ Ϫ0.81, P Ͻ 0.01) and a significant positive correlation between QUICKI and S i (r ϭ 0.89, r ϭ 0.90, and r ϭ 0.81, P Ͻ 0.01) at each time point. There was a significant positive correlation between FGIR and S i (r ϭ 0.91, r ϭ 0.91, and r ϭ 0.82, P Ͻ 0.01) and a significant negative correlation between fasting insulin and S i (r ϭ Ϫ90, r ϭ Ϫ0.90, and r ϭ Ϫ0.88, P Ͻ 0.01). HOMA-␤% was not as strongly correlated with AIR (r ϭ 0.60, r ϭ 0.54, and r ϭ 0.61, P Ͻ 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-␤%, 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. Diabetes Care 27:314 -319, 2004T he global increase in obesity in children and adolescents heightens the risk of insulin resistance and type 2 diabetes (1). Insulin resistance is proposed to have a pivotal role in the development of the metabolic syndrome ("Syndrome X") (2). Furthermore, clustering of cardiovascular risk factors is seen in children and adolescents with the highest degree of insulin resistance, suggesting that adult cardiovascular disease is more likely to develop in these young people (3,4). Hence, valid and reliable methods to measure insulin sensitivity in this atrisk population are essential to assess the presence and extent of insulin resistance, associated factors, progression over time, and the effect of pharmacological and lifestyle interventions.The modified minimal model frequently sampled intravenous glucose tolerance test (FSIVGTT) is a method that assesses insulin sensitivity by a compu...

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Vitamin D is synthesised in the skin through the action of UVB radiation (sunlight), and 25-hydroxy vitamin D (25OHD) measured in serum as a marker of vitamin D status. Several studies, mostly conducted in high latitudes, have shown an association between type 1 diabetes mellitus (T1DM) and low serum 25OHD. We conducted a case-control study to determine whether, in a sub-tropical environment with abundant sunlight (latitude 27.5°S), children with T1DM have lower serum vitamin D than children without diabetes. Fifty-six children with T1DM (14 newly diagnosed) and 46 unrelated control children participated in the study. Serum 25OHD, 1,25-dihydroxy vitamin D (1,25(OH)(2) D) and selected biochemical indices were measured. Vitamin D receptor (VDR) polymorphisms Taq1, Fok1, and Apa1 were genotyped. Fitzpatrick skin classification, self-reported daily hours of outdoor exposure, and mean UV index over the 35 d prior to blood collection were recorded. Serum 25OHD was lower in children with T1DM (n = 56) than in controls (n = 46) [mean (95%CI) = 78.7 (71.8-85.6) nmol/L vs. 91.4 (83.5-98.7) nmol/L, p = 0.02]. T1DM children had lower self-reported outdoor exposure and mean UV exposure, but no significant difference in distribution of VDR polymorphisms. 25OHD remained lower in children with T1DM after covariate adjustment. Children newly diagnosed with T1DM had lower 1,25(OH)(2) D [median (IQR) = 89 (68-122) pmol/L] than controls [121 (108-159) pmol/L, p = 0.03], or children with established diabetes [137 (113-153) pmol/L, p = 0.01]. Children with T1DM have lower 25OHD than controls, even in an environment of abundant sunlight. Whether low vitamin D is a risk factor or consequence of T1DM is unknown.