Previous cross-sectional studies show that puberty is associated with a reduction in insulin sensitivity (S_I), but no longitudinal studies have examined this change in detail. This study is a longitudinal study in 60 children (33 male and 27 female subjects; 32 Caucasian and 28 African-American) examined at Tanner stage I (age 9.2 ± 1.4 years) and after 2.0 ± 0.6 years of follow-up, by which time 29 children remained at Tanner stage I and 31 had progressed to Tanner stage III or IV. Tanner stage was assessed by physical examination. S_I, the acute insulin response (AIR), and the disposition index (DI) were determined by the tolbutamide-modified intravenous glucose tolerance test and minimal modeling, body fat mass was assessed by dual-energy X-ray absorptiometry, visceral fat was determined by computed tomography, and fasting blood was analyzed for hormone levels. In children progressing to Tanner stage III, S_I fell significantly by 32% (4.4 ± 3.0 to 3.0 ± 1.7 × 10⁻⁴min⁻¹/[μIU/ml]), AIR increased by 30%, DI fell by 27%, and there was a significant increase in fasting glucose (93.5 ± 5.0 to 97.0 ± 4.1 mg/dl) and insulin (14.3 ± 8.1 to 18.6 ± 11.0 μIU/ml). In children remaining at Tanner stage I, there was a slight increase in S_I (6.4 ± 3.1 to 7.4 ± 3.5 × 10⁻⁴min⁻¹/[μIU/ml]) with no significant change in AIR or fasting glucose and insulin. The pubertal fall in S_I was more consistent in African-Americans; remained significant after controlling for age, sex, and change in fat mass, visceral fat, and fat-free mass; and was similar in children at low, medium, and high body fat. Change in S_I was not significantly related to change in fasting hormone levels, but change in AIR was significantly related to change in androstendione (r = 0.39; P = 0.04). Pubertal transition from Tanner stage I to Tanner stage III was associated with a 32% reduction in S_I, and increases in fasting glucose, insulin, and AIR. These changes were similar across sex, ethnicity, and obesity. The significant fall in DI suggests conservation in β-cell function or an inadequate β-cell response to the fall in S_I. The fall in S_I was not associated with changes in body fat, visceral fat, IGF-I, androgens, or estradiol.

Overweight/obesity continues to increase in children and adolescents, and annual obesity-related hospital costs in 6-17 yr olds have reached 127 million dollars per year. Overweight children and adolescents are now being diagnosed with impaired glucose tolerance and type 2 diabetes, and they show early signs of the insulin resistance syndrome and cardiovascular risk. Several risk factors have been identified as contributors to the development of type 2 diabetes and cardiovascular risk in youth. These factors include increased body fat and abdominal fat, insulin resistance, ethnicity (with greater risk in African-American, Hispanic, and Native American children), and onset of puberty. There is no clear explanation of how these factors increase risk, but they appear to act in an additive fashion. We hypothesize that the constellation of these risk factors may be especially problematic during the critical period of adolescent development, especially in individuals who may have compromised beta-cell function and an inability to compensate for severe insulin resistance. Therefore, the purpose of this paper is to review the pathophysiology of type 2 diabetes and cardiovascular risk in obese children and adolescents.

Excess fructose consumption is hypothesized to be associated with risk for metabolic disease. Actual fructose consumption levels are difficult to estimate because of the unlabeled quantity of fructose in beverages. The aims of this study were threefold: 1) re-examine the fructose content in previously tested beverages using two additional assay methods capable of detecting other sugars, especially maltose, 2) compare data across all methods to determine the actual free fructose-to-glucose ratio in beverages made either with or without high-fructose corn syrup (HFCS), and 3) expand the analysis to determine fructose content in commonly consumed juice products. Sugar-sweetened beverages (SSBs) and fruit juice drinks that were either made with or without HFCS were analyzed in separate, independent laboratories via three different methods to determine sugar profiles. For SSBs, the three independent laboratory methods showed consistent and reproducible results. In SSBs made with HFCS, fructose constituted 60.6% ± 2.7% of sugar content. In juices sweetened with HFCS, fructose accounted for 52.1% ± 5.9% of sugar content, although in some juices made from 100% fruit, fructose concentration reached 65.35 g/L accounting for 67% of sugars. Our results provide evidence of higher than expected amounts of free fructose in some beverages. Popular beverages made with HFCS have a fructose-to-glucose ratio of approximately 60:40, and thus contain 50% more fructose than glucose. Some pure fruit juices have twice as much fructose as glucose. These findings suggest that beverages made with HFCS and some juices have a sugar profile very different than sucrose, in which amounts of fructose and glucose are equivalent. Current dietary analyses may underestimate actual fructose consumption.

OBJECTIVE—The objective of this study was to compare insulin resistance relative to body fat and the associated compensatory responses in 57 healthy children living in Los Angeles, California (14 Caucasians, 15 African-Americans, and 28 Hispanics). RESEARCH DESIGN AND METHODS—Insulin sensitivity and acute insulin response were determined by intravenous glucose tolerance test. Insulin secretion, hepatic insulin extraction, and insulin clearance were estimated by C-peptide and insulin modeling. RESULTS—Insulin sensitivity was significantly lower in Hispanics and African-Americans compared with Caucasian children, and acute insulin response was significantly higher in African-American children. No ethnic differences were noted in the first-phase secretion, but second-phase insulin secretion was significantly higher in Hispanic children than in African-American children (200 ± 53 vs. 289 ± 41 nmol/min; P = 0.03). The greater acute insulin response in African-Americans, despite lower secretion, was explained by a lower hepatic insulin extraction in African-Americans compared with Hispanics (36.6 ± 2.9 vs. 47.3 ± 2.2%; P = 0.0006). CONCLUSIONS—In conclusion, Hispanic and African-American children are more insulin resistant than Caucasian children, but the associated compensatory responses are different across ethnic groups.