摘要
肥胖症和相关的非传染性疾病(NCD)的患病率在全球范围内呈上升趋势。虽然现代生活方式要求通过肌肉活动减少代谢能量的通气,但这种生活方式的转变也使人们可以全天候无限量地购买食物,从而延长了高热量和高血糖负荷食品的日常饮食时间。这些情况促进了线粒体中碳底物可用性的高连续通量,并引起了不断的生物能转换。由于源自底物的还原当量的过量流动,被破坏的生物能环境增加了解偶联的呼吸作用,并减少了泛醌进入呼吸链。通过脂肪细胞生热而使解偶联质子梯度转移,将减轻自由基对线粒体和其他细胞器的破坏作用。白色脂肪组织(WAT)对米色脂肪组织(beAT)的自适应诱导已显示出通过beAT的解偶联蛋白1(UCP1)独立的生热作用,对葡萄糖氧化,ROS保护和线粒体功能保存具有有益作用。但是,适应不良的阶段最终可能会因持续不健康的生活方式而开始。在这种代谢僵局下,低氧和促炎环境会促进脂肪分解,继而发生代谢异常,包括胰岛素抵抗,全身性炎症和临床NCD进展。单一的干预措施不可能逆转所有这些复杂的相互作用。包括饮食,营养和所有可修改的生活方式干预措施在内的综合规程可能是减速,停止或逆转NCD病理生理过程的首选。
关键词: 肥胖,脂肪细胞,线粒体,生热,适应,适应不良,饮食,营养,生活方式。
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