IMPAIRED INSULIN-INDUCED SYMPATHETIC NEURAL ACTIVATION AND VASODILATION IN SKELETAL-MUSCLE IN OBESE HUMANS
IMPAIRED INSULIN-INDUCED SYMPATHETIC NEURAL ACTIVATION AND VASODILATION IN SKELETAL-MUSCLE IN OBESE HUMANS
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DOI：
10.1172/jci117242
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发表时间：
1994-06-01
影响因子：
15.9
通讯作者：
SCHERRER, U
中科院分区：
文献类型：
--
作者：
VOLLENWEIDER, P;RANDIN, D;SCHERRER, U
交感神经系统是代谢和心血管功能的重要调节机制，交感神经活动的改变可能在肥胖的病因和/或并发症中起作用。在瘦受试者中，胰岛素引起交感神经激活和骨骼肌血管舒张。在肥胖受试者中，这种血管舒张功能受损，进而可能导致胰岛素抵抗。为了研究骨骼肌对高胰岛素血症的交感神经和血管舒张反应之间的关系，我们同时测量了8名瘦子和8名肥胖受试者在基础和2小时高胰岛素（6 pmol/kg / min）血糖钳夹期间的肌肉交感神经活动（MSNA）和小腿血流。本研究的主要发现有两方面：肥胖受试者的空腹MSNA率高出2.2倍，而正常血糖高胰岛素血症使瘦受试者的MSNA增加一倍以上，使小腿血流量增加约30%，而肥胖受试者只有轻微的血管舒张和交感神经兴奋作用。相比之下，两种非胰岛素交感刺激在瘦人和肥胖者中引起了相当大的MSNA增加。我们得出结论，肥胖受试者的胰岛素抵抗与空腹MSNA增加和骨骼肌组织中交感神经对生理性高胰岛素血症的反应性的特异性损伤有关。
The sympathetic nervous system is an important regulatory mechanism of both metabolic and cardiovascular function, and altered sympathetic activity may play a role in the etiology and/or complications of obesity. In lean subjects, insulin evokes sympathetic activation and vasodilation in skeletal muscle. In obese subjects such vasodilation is impaired and, in turn, may contribute to insulin resistance. To examine the relationship between sympathetic and vasodilatory responses in skeletal muscle to hyperinsulinemia, we simultaneously measured muscle sympathetic nerve activity (MSNA) and calf blood flow at basal and during a 2-h hyperinsulinemic (6 pmol/kg per min) euglycemic clamp in eight lean and eight obese subjects. The major findings of this study are twofold: obese subjects had a 2.2 times higher fasting rate of MSNA, and euglycemic hyperinsulinemia, which more than doubled MSNA and increased calf blood flow by roughly 30% in lean subjects, had only a minor vasodilatory and sympathoexcitatory effect in obese subjects. In contrast, two non-insulin-sympathetic stimuli evoked comparably large increases in MSNA in lean and obese subjects. We conclude that insulin resistance in obese subjects is associated with increased fasting MSNA and a specific impairment of sympathetic neural responsiveness to physiological hyperinsulinemia in skeletal muscle tissue.