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绝经前女性线粒体脂肪酸氧化与体脂的关联。

Associations of Mitochondrial Fatty Acid Oxidation with Body Fat in Premenopausal Women.

作者信息

Warren Jonathan L, Gower Barbara A, Hunter Gary R, Windham Samuel T, Moellering Douglas R, Fisher Gordon

机构信息

Department of Nutrition Sciences, University of Alabama at Birmingham, 1720 2nd Avenue South, Birmingham, AL 35294, USA.

Department of Human Studies, University of Alabama at Birmingham, 1720 2nd Avenue South, Birmingham, AL 35294, USA.

出版信息

J Nutr Metab. 2017;2017:7832057. doi: 10.1155/2017/7832057. Epub 2017 Oct 24.

DOI:10.1155/2017/7832057
PMID:29204295
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5674507/
Abstract

Higher fatty acid (FA) oxidation rates have been reported in obese individuals compared to lean counterparts; however whether this reflects a shift in substrate-specific oxidative capacity at the level of the skeletal muscle mitochondria has not been examined. The purpose of this study was to test the hypothesis that in situ measures of skeletal muscle mitochondria FA oxidation would be positively associated with total body fat. Participants were 38 premenopausal women (BMI = 26.5 ± 4.3 kg/m). Total and regional fat were assessed by dual-energy X-ray absorptiometry (DXA). Mitochondrial FA oxidation was assessed in permeabilized myofibers using high-resolution respirometry and a palmitoyl carnitine substrate. We found positive associations of total fat mass with State 3 (ADP-stimulated respiration) ( = 0.379, < 0.05) and the respiratory control ratio (RCR, measure of mitochondrial coupling) ( = 0.348, < 0.05). When participants were dichotomized by high or low body fat percent, participants with high total body fat displayed a higher RCR compared to those with low body fat ( < 0.05). There were no associations between any measure of regional fat and mitochondrial FA oxidation independent of total fat mass. In conclusion, greater FA oxidation in obesity may reflect molecular processes that enhance FA oxidation capacity at the mitochondrial level.

摘要

据报道,与瘦人相比,肥胖个体的高级脂肪酸(FA)氧化率更高;然而,这是否反映了骨骼肌线粒体水平上底物特异性氧化能力的转变尚未得到研究。本研究的目的是检验以下假设:骨骼肌线粒体FA氧化的原位测量值与全身脂肪呈正相关。研究对象为38名绝经前女性(BMI = 26.5 ± 4.3 kg/m²)。采用双能X线吸收法(DXA)评估全身和局部脂肪。使用高分辨率呼吸测定法和棕榈酰肉碱底物评估通透化肌纤维中的线粒体FA氧化。我们发现,总脂肪量与状态3(ADP刺激的呼吸)(r = 0.379,P < 0.05)和呼吸控制率(RCR,线粒体偶联指标)(r = 0.348,P < 0.05)呈正相关。当根据高或低体脂百分比将参与者分为两组时,高全身脂肪的参与者与低体脂的参与者相比,RCR更高(P < 0.05)。在不考虑总脂肪量的情况下,任何局部脂肪测量值与线粒体FA氧化之间均无关联。总之,肥胖中更高的FA氧化可能反映了在分子水平上增强线粒体FA氧化能力的过程。

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本文引用的文献

1
Potential Causes of Elevated REE after High-Intensity Exercise.高强度运动后静息能量消耗升高的潜在原因。
Med Sci Sports Exerc. 2017 Dec;49(12):2414-2421. doi: 10.1249/MSS.0000000000001386.
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Your mitochondria are what you eat: a high-fat or a high-sucrose diet eliminates metabolic flexibility in isolated mitochondria from rat skeletal muscle.线粒体如你所食:高脂或高糖饮食会消除大鼠骨骼肌分离线粒体中的代谢灵活性。
Physiol Rep. 2017 Mar;5(6). doi: 10.14814/phy2.13207.
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Defects in mitochondrial efficiency and H2O2 emissions in obese women are restored to a lean phenotype with aerobic exercise training.
肥胖女性线粒体效率和过氧化氢排放的缺陷通过有氧运动训练恢复到瘦体型表型。
Diabetes. 2015 Jun;64(6):2104-15. doi: 10.2337/db14-1701. Epub 2015 Jan 20.
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Racial differences in peripheral insulin sensitivity and mitochondrial capacity in the absence of obesity.在不肥胖的情况下,外周胰岛素敏感性和线粒体容量的种族差异。
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Submaximal ADP-stimulated respiration is impaired in ZDF rats and recovered by resveratrol.ZDF 大鼠的次最大 ADP 刺激呼吸受损,白藜芦醇可使其恢复。
J Physiol. 2013 Dec 1;591(23):6089-101. doi: 10.1113/jphysiol.2013.259226. Epub 2013 Sep 30.
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Impaired skeletal muscle mitochondrial function in morbidly obese patients is normalized one year after bariatric surgery.肥胖症患者的骨骼肌线粒体功能受损,在接受减重手术后一年得到了恢复正常。
Surg Obes Relat Dis. 2013 Nov-Dec;9(6):936-41. doi: 10.1016/j.soard.2013.03.009. Epub 2013 Apr 18.
7
Mitochondrial lipid oxidation is impaired in cultured myotubes from obese humans.线粒体脂质氧化在肥胖人群的肌管培养物中受损。
Int J Obes (Lond). 2012 Aug;36(8):1025-31. doi: 10.1038/ijo.2011.201. Epub 2011 Oct 25.
8
The regulation and physiology of mitochondrial proton leak.线粒体质子漏的调节和生理学。
Physiology (Bethesda). 2011 Jun;26(3):192-205. doi: 10.1152/physiol.00046.2010.
9
Inhibiting myosin-ATPase reveals a dynamic range of mitochondrial respiratory control in skeletal muscle.抑制肌球蛋白-ATP 酶揭示了骨骼肌中线粒体呼吸控制的动态范围。
Biochem J. 2011 Jul 15;437(2):215-22. doi: 10.1042/BJ20110366.
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Human obesity is characterized by defective fat storage and enhanced muscle fatty acid oxidation, and trimetazidine gradually counteracts these abnormalities.人类肥胖的特征是脂肪储存缺陷和肌肉脂肪酸氧化增强,曲美他嗪逐渐逆转这些异常。
Am J Physiol Endocrinol Metab. 2011 Jul;301(1):E105-12. doi: 10.1152/ajpendo.00680.2010. Epub 2011 Apr 19.