مقاله انگلیسی رایگان در مورد تغذیه کتوز و میتوهورمونیز – هینداوی ۲۰۱۸

All cells of the human body require ATP as the fundamental energy source to support life. Because mitochondria produce the majority of ATP, impaired mitochondrial function is implicated in the majority of today’s most concerning chronic and degenerative health conditions including obesity, cardiovascular disease, cancer, diabetes, sarcopenia, and neurodegenerative diseases [1]. Much of this association between mitochondrial function and disease can be attributed to excessive mitochondrial production of reactive oxygen species (ROS) [2]. Although mitochondrial ROS (mtROS) are generally considered harmful, which is certainly the case at high concentrations, modest levels stimulate necessary biological processes such as proliferation, dierentiation, and immunity [3]. Adaptations that enhance resistance to oxidative stress are also induced by mtROS [3], possibly decreasing net ROS production during basal metabolism. )is adaptive response is called mitohormesis [4–۶] and is a promising mechanism through which lifestyle interventions that enhance mitochondrial function may, in turn, enhance resistance to chronic and degenerative diseases. By dramatically shifting energy metabolism towards ketogenesis and fatty acid oxidation, ketogenic diets are likely to have a profound eect on mitochondrial function. However, despite the rapidly growing amount of research on ketogenic diets and their eects on various disease states, only a small amount of this research has focused on mitochondrial function or oxidative stress. )e well-established increase in fat oxidation induced by a ketogenic diet [7, 8] clearly indicates prominent connection with mitochondrial function and, in turn, oxidative stress and mitohormesis [5, 6, 9]. )erefore, the purpose of this review is to describe the current, but limited, understanding of how ketogenic diets may aect mitochondrial function and resistance to oxidative stress, particularly within the context of extending human healthspan.