OBJECTIVE -This study aimed to establish whether total fat or central fat was related to measures of insulin in obese Hispanic children with a family history of type 2 diabetes.RESEARCH DESIGN AND METHODS -Subjects were 32 children aged 8 -13 years. Visceral fat and subcutaneous abdominal fat were determined by magnetic resonance imaging at the umbilicus and total body fat was determined by dual-energy X-ray absorptiometry. Insulin sensitivity (S i ) and acute insulin response (AIR) were determined by frequently sampled intravenous tolerance test with minimal modeling.RESULTS -Mean fasting glucose and insulin, S i , and AIR (Ϯ SD) were 5.3 Ϯ 0.3 mmol/l, 206 Ϯ 105 pmol/l, 11.8 Ϯ 5.7 [ϫ 10 Ϫ4 min -1 /(pmol/l)], and 17,175 Ϯ 9,695 (pmol/l ϫ 10 min), respectively. In multivariate regression analysis, total fat mass was independently and positively related to fasting insulin (P Ͻ 0.01) and negatively related to S i (P Ͻ 0.05) but was not related to AIR. Visceral fat was independently and positively related to fasting insulin (P Ͻ 0.05) and AIR (P Ͻ 0.01) and negatively related to S i (P Ͻ 0.001).CONCLUSIONS -These findings support the hypothesis that specific accumulation of visceral fat in addition to overall adiposity in Hispanic children increases the risk of type 2 diabetes.
Diabetes Care 25:1631-1636, 2002T he association between obesity and insulin resistance has been well documented, and it has been hypothesized that specific metabolic effects of visceral fat may explain this association (1). Support for a causal role of visceral fat causing insulin resistance has been shown in animal studies in which surgical removal of visceral fat in obese rats reversed insulin resistance (2) and in animal studies in aging rats in which the loss in visceral fat, as a consequence of caloric restriction, resulted in improvement in hepatic insulin sensitivity (S i ) (3).Visceral fat seems to be metabolically unique compared with subcutaneous abdominal fat. Bjorntorp (4) suggested that visceral fat results in hepatic insulin resistance via a "portal" effect of free fatty acids released by increased omental fat. The increased flux of fatty acids to the liver leads to increased hepatic glucose production (5, 6) and decreased hepatic insulin clearance, which in turn leads to insulin resistance and hyperinsulinemia. In children as in adults, central fat seems to be related to S i . However, the precise depot that is associated with S i is not entirely clear and may differ with obesity status (7-9).Although the relationship between central fat and S i has been widely studied in Caucasians, there are very few reports in the Hispanic population. Studies in Hispanic Americans may be important because both children and adults in this subgroup of the population are more obese (10,11), have higher waist-to-hip ratios (12,13), and have higher insulin levels (11) than Caucasians (13). In addition, Hispanic adults have been found to be more insulin-resistant than Caucasians (13) and have greater central distribution of fat (14) at similar le...