Non-insulin-mediated glucose uptake in human immunodeficiency virus-infected men.
Non-insulin-mediated glucose uptake in human immunodeficiency virus-infected men.
复制标题
人类免疫缺陷病毒感染男性中非胰岛素介导的葡萄糖摄取。
作者：
R. Heyligenberg;J. Romijn;M.J.T. Hommes;E. Endert;J. K. M. E. Schattenkerk;H. Sauerwein
1.获得性免疫缺陷综合征的代谢特征之一是正常血-高胰岛素钳夹研究证实的组织葡萄糖摄取增加，表明胰岛素敏感性增加。然而，这些结果也可能与获得性免疫缺陷综合征中非胰岛素介导的葡萄糖摄取增加的混杂效应有关，这将导致错误地推测胰岛素敏感性增加。为了研究获得性免疫缺陷综合征中非胰岛素介导的葡萄糖摄取对总组织葡萄糖摄取的贡献，我们在临床稳定的人类免疫缺陷病毒感染（疾病控制中心IV级）男性（n = 7）和健康受试者（n = 5）中进行了低胰岛素钳夹研究。在吸收后状态和生长抑素诱导的胰岛素减少症期间，在正常血糖（约5.3 mmol/l）和高血糖（约11 mmol/l）葡萄糖浓度下，通过预充、连续输注[3- 3 H]葡萄糖测量葡萄糖摄取。2.基础葡萄糖浓度（患者，5.2 +/- 0.1 mmol/l;对照组，5.3 +/- 0.1 mmol/l）和基础葡萄糖组织摄取（患者，15.9 +/- 0.5 mumol min-1 kg-1无脂肪质量;对照组，15.2 +/- 0.4 mumol min-1 kg-1无脂肪质量）在两组之间没有差异。3.在生长抑素输注期间，正常血糖的葡萄糖摄取，反映了非胰岛素介导的葡萄糖摄取，在患者和对照受试者中分别下降至82 +/- 3%和78 +/- 2%（不显著）。在高血糖（约11 mmol/l）伴持续胰岛素减少的情况下，两组间葡萄糖摄取无差异（患者，16.8 +/- 0.6 mumol min-1 kg-1无脂体重;对照组，16.1+/- 0.3 mumol min-1 kg-1无脂体重）。（250字处删节）
1. One of the metabolic features of acquired immunodeficiency syndrome is increased tissue glucose uptake documented by euglycaemic-hyperinsulinaemic clamp studies, suggesting increased insulin sensitivity. However, these results may also be related to the confounding effect of increased non-insulin-mediated glucose uptake in acquired immunodeficiency syndrome, which will result in an erroneously presumed increased insulin sensitivity. To study the contribution of non-insulin-mediated glucose uptake to total tissue glucose uptake in acquired immunodeficiency syndrome, we conducted a hypoinsulinaemic clamp study in clinically stable human immunodeficiency virus-infected (Centers for Disease Control class IV) men (n = 7) and healthy subjects (n = 5). Glucose uptake was measured by a primed, continuous infusion of [3-3H]glucose in the postabsorptive state and during somatostatin-induced insulinopenia at euglycaemic (approximately 5.3 mmol/l) and hyperglycaemic (approximately 11 mmol/l) glucose concentrations. 2. Basal glucose concentration (patients, 5.2 +/- 0.1 mmol/l; control subjects, 5.3 +/- 0.1 mmol/l) and basal glucose tissue uptake (patients, 15.9 +/- 0.5 mumol min-1 kg-1 fat-free mass; control subjects, 15.2 +/- 0.4 mumol min-1 kg-1 fat-free mass) were not different between the two groups. 3. Euglycaemic glucose uptake during somatostatin infusion, reflecting non-insulin-mediated glucose uptake, decreased to 82 +/- 3% in patients and 78 +/- 2% in control subjects (not significant). Under hyperglycaemic (approximately 11 mmol/l) conditions with sustained insulinopenia, no differences in glucose uptake existed between the two groups (patients, 16.8 +/- 0.6 mumol min-1 kg-1 fat-free mass; control subjects, 16.1+/- 0.3 mumol min-1 kg-1 fat-free mass).(ABSTRACT TRUNCATED AT 250 WORDS)