Non‐Alcoholic fatty liver disease (NAFLD) is the most common form of liver disease and is characterized by fat accumulation in the liver. Hypercaloric diets generally increase hepatic fat accumulation, whereas hypocaloric diets decrease liver fat content. In addition, there is evidence to suggest that moderate amounts of unsaturated fatty acids seems to be protective for the development of a fatty liver, while consumption of saturated fatty acids (SFA) appears to predispose toward hepatic steatosis. Recent studies highlight a key role for mitochondrial dysfunction in the development and progression of NAFLD. It is proposed that changes in mitochondrial structure and function are key mechanisms by which SFA lead to the development and progression of NAFLD. In this review, it is described how SFA intake is associated with liver steatosis and decreases the efficiency of the respiratory transport chain. This results in the production of reactive oxygen species and damage to nearby structures, eventually leading to inflammation, apoptosis, and scarring of the liver. Furthermore, studies demonstrating that SFA intake affects the composition of mitochondrial membranes are presented, and this process accelerates the progression of NAFLD. It is likely that events are intertwined and reinforce each other, leading to a constant deterioration in health.

中文翻译：

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线粒体功能障碍是将饱和脂肪摄入量与 NAFLD 的发展和进展联系起来的关键途径。

非酒精性脂肪性肝病 (NAFLD) 是最常见的肝脏疾病，其特征是脂肪在肝脏中堆积。高热量饮食通常会增加肝脏脂肪堆积，而低热量饮食会降低肝脏脂肪含量。此外，有证据表明适量的不饱和脂肪酸似乎对脂肪肝的发展有保护作用，而饱和脂肪酸 (SFA) 的摄入似乎易导致肝脂肪变性。最近的研究强调了线粒体功能障碍在 NAFLD 的发展和进展中的关键作用。提出线粒体结构和功能的变化是 SFA 导致 NAFLD 发展和进展的关键机制。在这次审查中，描述了 SFA 摄入如何与肝脏脂肪变性相关并降低呼吸运输链的效率。这会导致活性氧的产生和对附近结构的损害，最终导致炎症、细胞凋亡和肝脏瘢痕形成。此外，研究表明 SFA 摄入会影响线粒体膜的组成，并且该过程加速了 NAFLD 的进展。事件很可能相互交织并相互加强，导致健康状况不断恶化。研究表明，SFA 摄入会影响线粒体膜的组成，而这一过程会加速 NAFLD 的进展。事件很可能相互交织并相互加强，导致健康状况不断恶化。研究表明，SFA 摄入会影响线粒体膜的组成，而这一过程会加速 NAFLD 的进展。事件很可能相互交织并相互加强，导致健康状况不断恶化。