Petersen Anne Marie Winther, Magkos Faidon, Atherton Philip, Selby Anna, Smith Kenneth, Rennie Michael J, Pedersen Bente Klarlund, Mittendorfer Bettina
Centre of Inflammation and Metabolism, Department of Infectious Diseases and Copenhagen Muscle Research Centre, Copenhagen, Denmark.
Am J Physiol Endocrinol Metab. 2007 Sep;293(3):E843-8. doi: 10.1152/ajpendo.00301.2007. Epub 2007 Jul 3.
Smoking causes multiple organ dysfunction. The effect of smoking on skeletal muscle protein metabolism is unknown. We hypothesized that the rate of skeletal muscle protein synthesis is depressed in smokers compared with non-smokers. We studied eight smokers (> or =20 cigarettes/day for > or =20 years) and eight non-smokers matched for sex (4 men and 4 women per group), age (65 +/- 3 and 63 +/- 3 yr, respectively; means +/- SEM) and body mass index (25.9 +/- 0.9 and 25.1 +/- 1.2 kg/m(2), respectively). Each subject underwent an intravenous infusion of stable isotope-labeled leucine in conjunction with blood and muscle tissue sampling to measure the mixed muscle protein fractional synthesis rate (FSR) and whole body leucine rate of appearance (Ra) in plasma (an index of whole body proteolysis), the expression of genes involved in the regulation of muscle mass (myostatin, a muscle growth inhibitor, and MAFBx and MuRF-1, which encode E3 ubiquitin ligases in the proteasome proteolytic pathway) and that for the inflammatory cytokine TNF-alpha in muscle, and the concentration of inflammatory markers in plasma (C-reactive protein, TNF-alpha, interleukin-6) which are associated with muscle wasting in other conditions. There were no differences between nonsmokers and smokers in plasma leucine concentration, leucine rate of appearance, and plasma concentrations of inflammatory markers, or TNF-alpha mRNA in muscle, but muscle protein FSR was much less (0.037 +/- 0.005 vs. 0.059 +/- 0.005%/h, respectively, P = 0.004), and myostatin and MAFBx (but not MuRF-1) expression were much greater (by approximately 33 and 45%, respectivley, P < 0.05) in the muscle of smokers than of nonsmokers. We conclude that smoking impairs the muscle protein synthesis process and increases the expression of genes associated with impaired muscle maintenance; smoking therefore likely increases the risk of sarcopenia.
吸烟会导致多器官功能障碍。吸烟对骨骼肌蛋白质代谢的影响尚不清楚。我们推测，与不吸烟者相比，吸烟者骨骼肌蛋白质合成速率会降低。我们研究了8名吸烟者（每天吸烟≥20支，持续≥20年）和8名性别匹配的不吸烟者（每组4名男性和4名女性），年龄（分别为65±3岁和63±3岁；均值±标准误）和体重指数（分别为25.9±0.9和25.1±1.2kg/m²）。每位受试者接受静脉输注稳定同位素标记的亮氨酸，并同时采集血液和肌肉组织样本，以测量混合肌肉蛋白质分数合成率（FSR）和血浆中全身亮氨酸出现率（Ra）（全身蛋白水解的指标）、参与肌肉质量调节的基因（肌肉生长抑制因子肌生成抑制素、以及在蛋白酶体蛋白水解途径中编码E3泛素连接酶的MAFBx和MuRF-1）在肌肉中的表达，以及肌肉中炎性细胞因子TNF-α的表达，还有血浆中与其他情况下肌肉消耗相关的炎性标志物（C反应蛋白、TNF-α、白细胞介素-6）的浓度。不吸烟者和吸烟者在血浆亮氨酸浓度、亮氨酸出现率、血浆炎性标志物浓度或肌肉中TNF-αmRNA方面没有差异，但肌肉蛋白质FSR要低得多（分别为0.037± .005 vs. 0.059±0.005%/小时，P = 0.004），并且吸烟者肌肉中肌生成抑制素和MAFBx（但不包括MuRF-1）的表达比不吸烟者高得多（分别约高33%和45%，P < 0.05）。我们得出结论，吸烟会损害肌肉蛋白质合成过程，并增加与肌肉维持受损相关基因的表达；因此，吸烟可能会增加肌肉减少症的风险。
