Mitochondrial Dysfunction is a Key Pathway that Links Saturated Fat Intake to the Development and Progression of NAFLD

• Published in: Molecular nutrition & food research Vol. 65; no. 1; pp. e1900942 - n/a
• Main Authors: Meex, Ruth C. R., Blaak, Ellen E.
• Format: Journal Article
• Language: English
• Published: Germany Wiley Subscription Services, Inc 01-01-2021; John Wiley and Sons Inc
• Subjects: Accumulation; Adenosine Triphosphate - metabolism; Animals; Apoptosis; Diet; Dietary Fats - adverse effects; Dietary Fats - pharmacokinetics; Endoplasmic Reticulum Stress; Fatty acids; Fatty Acids - adverse effects; Fatty Acids - pharmacokinetics; Fatty liver; human intervention studies; Humans; Hypocaloric diet; Inflammation; Liver; Liver diseases; Mitochondria; Mitochondria, Liver - chemistry; Mitochondria, Liver - drug effects; Mitochondria, Liver - metabolism; Mitochondria, Liver - pathology; mitochondrial dysfunction; Non-alcoholic Fatty Liver Disease - etiology; Non-alcoholic Fatty Liver Disease - pathology; non‐alcoholic fatty liver disease; nutrition; Reactive oxygen species; Reactive Oxygen Species - metabolism; Review; Reviews; saturated fatty acids; Scars; Steatosis; Structural damage; Structure-function relationships; nutrition; mitochondrial dysfunction; saturated fatty acids; human intervention studies; non-alcoholic fatty liver disease
• ISSN: 1613-4125; 1613-4133
• DOI: 10.1002/mnfr.201900942

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.
Mitochondrial dysfunction is a key mechanism by which saturated fatty acids (SFA) result in the development and progression of non‐alcoholic fatty liver disease (NAFLD). SFA increases liver fat, decreases the efficiency of the respiratory transport chain and results in the production of reactive oxygen species and endoplasmatic reticulum stress. SFA also affect the composition of mitochondrial membranes. These processes lead inflammation, apoptosis, and scarring of the liver.