Metz Lore, Mercier Jacques, Tremblay Angelo, Alméras Natalie, Joanisse Denis R
Département de Physiologie des Interactions EA 701 Muscles et Pathologies chroniques, Institut de biologie, Montpellier, France.
J Appl Physiol (1985). 2008 Mar;104(3):633-8. doi: 10.1152/japplphysiol.00681.2007. Epub 2007 Dec 13.
The effects of weight loss on skeletal muscle lactate transporter [monocarboxylate transporter (MCT)] expression in obese subjects were investigated to better understand how lactate transporter metabolism is regulated in insulin-resistant states. Ten obese subjects underwent non-macronutrient-specific energy restriction for 15 wk. Anthropometric measurements and a needle biopsy of the vastus lateralis muscle before and after the weight loss program were performed. Enzymatic activity, fiber type distribution, and skeletal muscle MCT protein expression were measured. Muscle from nonobese control subjects was used for comparison of MCT levels. The program induced a weight loss of 9.2 +/- 1.6 kg. Compared with controls, muscle from obese subjects showed a strong tendency (P = 0.06) for elevated MCT4 expression (+69%) before the weight loss program. MCT4 expression decreased (-7%) following weight loss to reach levels that were not statistically different from control levels. There were no differences in MCT1 expression between controls and obese subjects before and after weight loss. A highly predictive regression model (R2 = 0.93), including waist circumference, citrate synthase activity, and percentage of type 1 fibers, was found to explain the highly variable MCT1 response to weight loss in the obese group. Therefore, in obesity, MCT1 expression appears linked both to changes in oxidative parameters and to changes in visceral adipose tissue content. The strong tendency for elevated expression of muscle MCT4 could reflect the need to release greater amounts of muscle lactate in the obese state, a situation that would be normalized with weight loss as indicated by decreased MCT4 levels.
为了更好地理解在胰岛素抵抗状态下乳酸转运体代谢是如何被调节的，研究了体重减轻对肥胖受试者骨骼肌乳酸转运体[单羧酸转运体（MCT）]表达的影响。十名肥胖受试者进行了为期15周的非特定宏量营养素能量限制。在体重减轻计划前后进行人体测量和股外侧肌的针吸活检。测量酶活性、纤维类型分布和骨骼肌MCT蛋白表达。使用非肥胖对照受试者的肌肉来比较MCT水平。该计划导致体重减轻了9.2±1.6千克。与对照组相比，肥胖受试者的肌肉在体重减轻计划前显示出MCT4表达升高（+69%）的强烈趋势（P = 0.06）。体重减轻后MCT4表达下降（-7%），达到与对照水平无统计学差异的水平。在体重减轻前后，对照组和肥胖受试者之间的MCT1表达没有差异。发现一个高度预测性的回归模型（R2 = 0.93），包括腰围、柠檬酸合酶活性和1型纤维百分比，可以解释肥胖组中MCT1对体重减轻的高度可变反应。因此，在肥胖状态下，MCT1表达似乎既与氧化参数的变化有关，也与内脏脂肪组织含量的变化有关。肌肉MCT4表达升高的强烈趋势可能反映了肥胖状态下释放更多肌肉乳酸的需要，而体重减轻后MCT4水平下降表明这种情况会恢复正常。
