Sinha Ranjana, Fisch Gene, Teague Barbara, Tamborlane William V, Banyas Bruna, Allen Karin, Savoye Mary, Rieger Vera, Taksali Sara, Barbetta Gina, Sherwin Robert S, Caprio Sonia
Department of Pediatrics, Yale University School of Medicine, New Haven, Conn 06520, USA.
N Engl J Med. 2002 Mar 14;346(11):802-10. doi: 10.1056/NEJMoa012578.
Childhood obesity, epidemic in the United States, has been accompanied by an increase in the prevalence of type 2 diabetes among children and adolescents. We determined the prevalence of impaired glucose tolerance in a multiethnic cohort of 167 obese children and adolescents.
All subjects underwent a two-hour oral glucose-tolerance test (1.75 g [DOSAGE ERROR CORRECTED] of glucose per kilogram of body weight), and glucose, insulin, and C-peptide levels were measured. Fasting levels of proinsulin were obtained, and the ratio of proinsulin to insulin was calculated. Insulin resistance was estimated by homeostatic model assessment, and beta-cell function was estimated by calculating the ratio between the changes in the insulin level and the glucose level during the first 30 minutes after the ingestion of glucose.
Impaired glucose tolerance was detected in 25 percent of the 55 obese children (4 to 10 years of age) and 21 percent of the 112 obese adolescents (11 to 18 years of age); silent type 2 diabetes was identified in 4 percent of the obese adolescents. Insulin and C-peptide levels were markedly elevated after the glucose-tolerance test in subjects with impaired glucose tolerance but not in adolescents with diabetes, who had a reduced ratio of the 30-minute change in the insulin level to the 30-minute change in the glucose level. After the body-mass index had been controlled for, insulin resistance was greater in the affected cohort and was the best predictor of impaired glucose tolerance.
Impaired glucose tolerance is highly prevalent among children and adolescents with severe obesity, irrespective of ethnic group. Impaired oral glucose tolerance was associated with insulin resistance while beta-cell function was still relatively preserved. Overt type 2 diabetes was linked to beta-cell failure.
儿童肥胖在美国呈流行态势，与此同时儿童和青少年2型糖尿病的患病率也有所上升。我们在一个多民族队列中对167名肥胖儿童和青少年进行了糖耐量受损情况的测定。
所有受试者均接受了两小时口服葡萄糖耐量试验（每千克体重1.75克[剂量已校正]葡萄糖），并测定了血糖、胰岛素和C肽水平。获取胰岛素原的空腹水平，并计算胰岛素原与胰岛素的比值。通过稳态模型评估来估算胰岛素抵抗，通过计算摄入葡萄糖后最初30分钟内胰岛素水平变化与血糖水平变化的比值来估算β细胞功能。
在55名肥胖儿童（4至10岁）中，25%检测出糖耐量受损；在112名肥胖青少年（11至18岁）中，21%检测出糖耐量受损；在肥胖青少年中，4%被诊断为隐匿性2型糖尿病。糖耐量受损的受试者在葡萄糖耐量试验后胰岛素和C肽水平显著升高，但糖尿病青少年则不然，他们胰岛素水平30分钟变化与血糖水平30分钟变化的比值降低。在对体重指数进行校正后，患病队列中的胰岛素抵抗更强，且是糖耐量受损的最佳预测指标。
无论种族如何，糖耐量受损在重度肥胖的儿童和青少年中都极为普遍。口服糖耐量受损与胰岛素抵抗相关，而β细胞功能仍相对保留。显性2型糖尿病与β细胞功能衰竭有关。
