Stoppoloni G, Prisco F, Alfano C, Iafusco D, Marrazzo G, Paolisso G
Istituto di Clinica Pediatrica, 1st Medical School, University of Naples, Italy.
Diabete Metab. 1990 Jul-Aug;16(4):267-71.
The characteristics of insulin resistance, in Turner syndrome are still unclear. For this purpose in 4 patients with Turner syndrome and in 8 control females we performed an euglycaemic hyperinsulinemic glucose clamp at the following insulin infusion rates (50 and 100 mU/Kg x h), each period lasting 120 min. A simultaneous infusion of D-3-H-glucose allowed us to determine in basal conditions and during the clamp hepatic glucose output and glucose disappearance rate (Rd). In basal conditions plasma glucose (4.8 +/- 0.1 vs 4.6 +/- 0.2 mmol/1 p = NS) and plasma glucagon (102 +/- 7.5 vs 112 +/- 11.3 ng/l p = NS) were similar in both groups despite higher plasma insulin (19 +/- 1.8 vs 7 +/- 2.2 mU/l p less than 0.05) and C-peptide (1.0 less than 0.1 vs 0.8 +/- 0.06 pmol/l p less than 0.05) levels in patients with Turner syndrome. In the last 60 min of the lower insulin infusion rate glucose infusion rate (4.1 +/- 0.3 vs 2.9 +/- 0.4 mg/Kg x min p less than 0.05) and glucose disappearance rate (3.89 +/- 0.12 vs 2.63 +/- 0.11 mg/Kg x min p less than 0.01) were significantly reduced in patients with Turner. On the contrary hepatic glucose output was similarly suppressed in both groups of subjects. Doubling the insulin infusion rate, we obtained similar results in patients and controls respectively. So we conclude that in Turner syndrome the insulin resistance state is mainly due to a muscular receptor defect.
特纳综合征中胰岛素抵抗的特征仍不明确。为此，我们对4例特纳综合征患者和8例对照女性进行了正常血糖高胰岛素葡萄糖钳夹试验，胰岛素输注速率如下（50和100 mU/Kg×h），每个阶段持续120分钟。同时输注D-3-H-葡萄糖使我们能够在基础状态和钳夹期间测定肝脏葡萄糖输出和葡萄糖消失率（Rd）。在基础状态下，两组的血浆葡萄糖（4.8±0.1对4.6±0.2 mmol/L，p=无显著性差异）和血浆胰高血糖素（102±7.5对112±11.3 ng/L，p=无显著性差异）相似，尽管特纳综合征患者的血浆胰岛素（19±1.8对7±2.2 mU/L，p<0.05）和C肽（1.0±0.1对0.8±0.06 pmol/L，p<0.05）水平较高。在较低胰岛素输注速率的最后60分钟，特纳综合征患者的葡萄糖输注速率（4.1±0.3对2.9±0.4 mg/Kg×min，p<0.05）和葡萄糖消失率（3.89±0.12对2.63±0.11 mg/Kg×min，p<0.01）显著降低。相反，两组受试者的肝脏葡萄糖输出受到类似抑制。将胰岛素输注速率加倍后，我们在患者和对照组中分别获得了相似的结果。因此我们得出结论，在特纳综合征中，胰岛素抵抗状态主要是由于肌肉受体缺陷所致。
