Virkamäki A, Puhakainen I, Koivisto V A, Vuorinen-Markkola H, Yki-Järvinen H
Second Department of Medicine, Helsinki University, Finland.
J Clin Endocrinol Metab. 1992 Mar;74(3):673-9. doi: 10.1210/jcem.74.3.1740504.
To examine mechanisms of insulin resistance, nine patients (age 33 +/- 4 yr, body mass index 22 +/- 1 kg/m2) with acute bacterial or viral infections and in six matched normal subjects were studied. Endogenous glucose appearance (Ra), glucose disappearance (Rd), and recycling, the percentage of plasma lactate originating from plasma glucose, total glucose oxidation, and whole body and forearm muscle Rd were measured after an overnight fast in the basal state and during physiological hyperinsulinemia (serum insulin approximately 215 pmol/L). Basally Ra, Rd, glucose recycling, and oxidation were similar in both groups. During hyperinsulinemia, insulin stimulated plasma Rd approximately 35% less (17.6 +/- 1.3 vs. 26.8 +/- 3.6 mumol/kg.min, P less than 0.01, patients vs. normal subjects), and inhibited endogenous Ra less in the patients (from 13.3 +/- 0.8 to 5.3 +/- 0.8 mumol/kg.min) than in the normal subjects (from 12.8 +/- 1.0 to 2.1 +/- 1.2 mumol/kg.min, P less than 0.01). The decrease in whole body Rd was largely explained by a approximately 75% reduction in muscle Rd (5.6 +/- 1.5 vs. 20.8 +/- 3.3 mumol/kg muscle.min, P less than 0.01, patients vs. normal subjects). The defect in Rd was confined to nonoxidative (4.8 +/- 1.1 vs. 11.0 +/- 3.0 mumol/kg.min, P less than 0.01, patients vs. normal subjects) but not to oxidative glucose metabolism. The percentage of plasma lactate derived from plasma glucose during hyperinsulinemia averaged 63 +/- 6% in the patients and 79 +/- 5% in the normal subjects, indicating that glycogenolysis did not excessively dilute glycolytic carbons in the patients. We conclude that during natural infections in humans, abnormal glucose metabolism is confined to the insulin-stimulated state and involves a marked defect in muscle glucose uptake and glycogen synthesis, as well as a less marked hepatic defect.
为研究胰岛素抵抗的机制，我们对9例急性细菌或病毒感染患者（年龄33±4岁，体重指数22±1kg/m²）和6例匹配的正常受试者进行了研究。在基础状态下过夜禁食后以及生理性高胰岛素血症期间（血清胰岛素约215pmol/L），测量内源性葡萄糖生成率（Ra）、葡萄糖消失率（Rd）、再循环率（即血浆乳酸中源自血浆葡萄糖的百分比）、总葡萄糖氧化率以及全身和前臂肌肉的Rd。基础状态下，两组的Ra、Rd、葡萄糖再循环率和氧化率相似。在高胰岛素血症期间，胰岛素刺激的血浆Rd在患者中比正常受试者低约35%（17.6±1.3对26.8±3.6μmol/kg·min，P<0.01，患者与正常受试者相比），并且患者中胰岛素对内源性Ra的抑制作用比正常受试者小（从13.3±0.8降至5.3±0.8μmol/kg·min）（从12.8±1.0降至2.1±1.2μmol/kg·min，P<0.01）。全身Rd的降低主要是由于肌肉Rd降低了约75%（5.6±1.5对20.8±3.3μmol/kg肌肉·min，P<0.01，患者与正常受试者相比）。Rd的缺陷局限于非氧化途径（4.8±1.1对11.0±3.0μmol/kg·min，P<0.01，患者与正常受试者相比），但不涉及氧化葡萄糖代谢。在高胰岛素血症期间，患者血浆乳酸中源自血浆葡萄糖的百分比平均为63±6%，正常受试者为79±5%，这表明患者中糖原分解并未过度稀释糖酵解碳。我们得出结论，在人类自然感染期间，异常的葡萄糖代谢仅限于胰岛素刺激状态，涉及肌肉葡萄糖摄取和糖原合成的明显缺陷以及肝脏的较不明显缺陷。
