Council for Nutritional and Environmental Medicine (CONEM), Mo i Rana, Norway.
Doctor of Philosophy Program in Nutrition, Faculty of Medicine Ramathibodi Hospital and Institute of Nutrition, Mahidol University, Bangkok, Thailand.
Curr Med Chem. 2021;28(9):1683-1702. doi: 10.2174/0929867327666200505090449.
The obesity and the associated non-communicable diseases (NCDs) are globally increasing in their prevalence. While the modern-day lifestyle required less ventilation of metabolic energy through muscular activities, this lifestyle transition also provided the unlimited accession to foods around the clock, which prolong the daily eating period of foods that contained high calorie and high glycemic load. These situations promote the high continuous flux of carbon substrate availability in mitochondria and induce the indecisive bioenergetic switches. The disrupted bioenergetic milieu increases the uncoupling respiration due to the excess flow of the substrate-derived reducing equivalents and reduces ubiquinones into the respiratory chain. The diversion of the uncoupling proton gradient through adipocyte thermogenesis will then alleviate the damaging effects of free radicals to mitochondria and other organelles. The adaptive induction of white adipose tissues (WAT) to beige adipose tissues (beAT) has shown beneficial effects on glucose oxidation, ROS protection and mitochondrial function preservation through the uncoupling protein 1 (UCP1)-independent thermogenesis of beAT. However, the maladaptive stage can eventually initiate with the persistent unhealthy lifestyles. Under this metabolic gridlock, the low oxygen and pro-inflammatory environments promote the adipose breakdown with sequential metabolic dysregulation, including insulin resistance, systemic inflammation and clinical NCDs progression. It is unlikely that a single intervention can reverse all these complex interactions. A comprehensive protocol that includes dietary, nutritional and all modifiable lifestyle interventions, can be the preferable choice to decelerate, stop, or reverse the NCDs pathophysiologic processes.
肥胖症和相关的非传染性疾病(NCDs)在全球范围内的患病率正在不断增加。虽然现代生活方式需要通过肌肉活动来减少代谢能量的通风,但这种生活方式的转变也提供了无限的机会来随时获取食物,这延长了日常进食富含高热量和高血糖负荷的食物的时间。这些情况促进了线粒体中碳底物可用性的持续高速通量,并诱导了不确定的生物能量转换。由于底物衍生的还原当量的过剩流动以及将泛醌减少到呼吸链中,破坏的生物能量环境会增加解偶联呼吸。通过脂肪细胞产热,解偶联质子梯度的转移将减轻自由基对线粒体和其他细胞器的损害作用。白色脂肪组织(WAT)向米色脂肪组织(beAT)的适应性诱导通过 beAT 的解偶联蛋白 1(UCP1)非依赖性产热,显示出对葡萄糖氧化、ROS 保护和线粒体功能保存的有益影响。然而,随着持续的不健康生活方式,适应性阶段最终可能会开始。在这种代谢僵局下,低氧和促炎环境促进脂肪分解,随后出现代谢失调,包括胰岛素抵抗、全身炎症和临床 NCDs 进展。单一干预措施不太可能逆转所有这些复杂的相互作用。包括饮食、营养和所有可改变的生活方式干预在内的综合方案,可能是减缓、停止或逆转 NCDs 病理生理过程的首选。