论文部分内容阅读
肥胖是胰岛素抵抗发生的一个重要危险因素。初始代偿机制包括胰岛素水平增加,该现象被认为可诱发交感神经兴奋,以试图恢复能量平衡。但之前研究者报道肥胖时交感神经兴奋对静息能量消耗并无有益作用。相反,研究者假设交感神经兴奋导致胰岛素抵抗。为验证此假设,研究者采用标准的高胰岛素葡萄糖平衡钳夹方法评估肥胖患者胰岛素敏感性。以交叉设计方案将肥胖患者随机分配至生理盐水组(对照日)
Obesity is an important risk factor for insulin resistance. Initial compensatory mechanisms, including increased insulin levels, are thought to induce sympathetic excitation in an attempt to restore energy balance. However, previous researchers reported that sympathetic activity during obesity had no beneficial effect on resting energy expenditure. In contrast, researchers hypothesized that sympathetic excitation leads to insulin resistance. To test this hypothesis, we evaluated insulin sensitivity in obese patients using a standard high-insulin glucose balance clamp. Obese patients were randomly assigned to saline group (crossover design)