Cerutti F, Sacchetti C, Bessone A, Rabbone I, Cavallo-Perin P, Pacini G
Department of Pediatrics, University of Turin, Italy.
Acta Paediatr. 1998 Oct;87(10):1045-50. doi: 10.1080/080352598750031356.
Obesity is characterized by variable degrees of hyperinsulinaemia, which has been attributed to either beta-cell hypersecretion or reduced hepatic insulin extraction, or both. To investigate this controversial issue, a 4-h frequently sampled i.v. glucose tolerance test (glucose dose 12.8 g m(-2)) was performed in 13 normotolerant, grossly obese adolescents (10 F/3 M; 13+/-1 y; body mass index 32+/-0.9; pubertal stage 4-5; obesity duration 7.8+/-3 y) and in a comparable group of 8 healthy, normal-weight subjects. Glucose, insulin and C-peptide time-course were analysed by the minimal model technique, which estimates beta-cell secretion, insulin sensitivity (Si), glucose effectiveness (SG) and hepatic insulin extraction (HE). Despite similar fasting and after load glucose patterns (SG similar in the two groups), obese adolescents showed sustained peripheral hyperinsulinaemia (total insulin area under the concentration curve 67.2+/-10.8 vs 19.1+/-1.2 pmol l(-1) in 240 min; p <0.002) and a 71% reduction in Si (2.02+/-0.33 vs 6.95+/-1.03 x 10(4) min(-1) (microU ml(-1)); p < 0.001). Compared with control subjects, the total amounts of prehepatic insulin secretion and posthepatic insulin delivery were also increased significantly in obese adolescents by 30% and 46%, respectively; HE was reduced by 15% during the first 30 min of the test, but recovered within the normal range during the rest of the test. In conclusion, severely obese adolescents are insulin resistant and their hyperinsulinaemia is primarily caused by beta-cell hypersecretion, whereas the reduction in insulin hepatic extraction is a transient metabolic phenomenon.
肥胖的特征是不同程度的高胰岛素血症，这归因于β细胞分泌过多或肝脏胰岛素摄取减少，或两者兼而有之。为了研究这个有争议的问题，对13名糖耐量正常、严重肥胖的青少年（10名女性/3名男性；13±1岁；体重指数32±0.9；青春期4-5期；肥胖持续时间7.8±3年）和8名健康、体重正常的对照者进行了4小时频繁采样的静脉葡萄糖耐量试验（葡萄糖剂量12.8 g m(-2)）。通过最小模型技术分析葡萄糖、胰岛素和C肽的时间进程，该技术可估计β细胞分泌、胰岛素敏感性（Si）、葡萄糖有效性（SG）和肝脏胰岛素摄取（HE）。尽管两组的空腹和负荷后血糖模式相似（两组的SG相似），但肥胖青少年表现出持续的外周高胰岛素血症（浓度曲线下的总胰岛素面积在240分钟内为67.2±10.8 vs 19.1±1.2 pmol l(-1)；p<0.002），Si降低了71%（2.02±0.33 vs 6.95±1.03 x 10(4) min(-1)（微U/ml(-1)）；p<0.001）。与对照组相比，肥胖青少年肝前胰岛素分泌总量和肝后胰岛素输送总量也分别显著增加了30%和46%；在试验的前30分钟内，HE降低了15%，但在试验的其余时间内恢复到正常范围。总之，严重肥胖的青少年存在胰岛素抵抗，他们的高胰岛素血症主要由β细胞分泌过多引起，而肝脏胰岛素摄取的减少是一种短暂的代谢现象。
