Journal Article Review Epublish
PubMed: 40535646 DOI: 10.62347/ZWSR4476
Role of gut-brain axis dysregulation in the pathogenesis of non-alcoholic fatty liver disease: mechanisms and therapeutic implications.
Am J Transl Res 17(5):3276-3292
Authors: Mei Wan, Weimin Zhao, Yifan Cai, Qian He, Jun Zeng
Affiliations
- The First Clinical Medical College of China Three Gorges University, Department of Endocrinology, Institute of Endocrine and Metabolic Diseases, Yichang Central People's Hospital Yichang 443000, Hubei, China.
- The First Clinical Medical College of China Three Gorges University, Department of Endocrinology, Institute of Endocrine and Metabolic Diseases, Yichang Central People's Hospital Yichang 443000, Hubei, China. Yichang Key Laboratory of Endocrinology Yichang 443000, Hubei, China.
- Life Science, Queen's University Kingston K7L 3N6, Ontario, Canada.
- Laboratory of Metabolic Bone Diseases, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University Changsha 410011, Hunan, China.
Abstract
Non-alcoholic fatty liver disease (NAFLD) has emerged as a global health challenge due to its rising prevalence and strong association with metabolic syndrome. Recent studies highlight the critical role of the gut-brain axis (GBA)-a bidirectional communication system between the gut, brain, and liver-in NAFLD pathogenesis. Dysregulation of this axis can worsen metabolic dysfunction, inflammation, and liver injury. This review discusses the mechanisms driving GBA dysregulation in NAFLD, including alterations in gut microbiota, increased intestinal permeability, neuroinflammation, and imbalances in the autonomic nervous system (ANS). We also explore therapeutic strategies, such as microbiota modulation, vagus nerve stimulation, and neuroprotective interventions, that may help mitigate the effects of GBA dysfunction on NAFLD progression.
MeSH
Liver Diseases, Non-Alcoholic Fatty Liver Disease, Brain, Liver, Alcoholics, Therapeutics, Fatty Liver, Fatty Liver, Alcoholic, Microbiota