“Regulation of adipose-derived fatty acid flux to the liver”-Impact on metabolic dysfunction-associated steatotic liver disease

Obesity is now considered a global epidemic, increasing the prevalence of obesity-related metabolic disorders. Obesity is characterized by an increase in white adipose tissue (WAT) mass that induce local inflammation and insulin resistance in the WAT, causing dysregulation of whole-body homeostasis. WAT is the primary organ for energy storage in the form of triacylglycerols, which are released as fatty acids (FAs) upon energy demand, a process named lipolysis. Under chronic high energy intake, adipocytes can expand to accommodate more triacylglycerols but when the storage capacity is impaired or lipolysis is dysregulated, FAs are redirected to other organs. The systemic overload of FAs contributes to the development of obesity-associated metabolic complications such as metabolic dysfunction-associated steatotic fatty liver disease (MASLD), formerly named non-alcoholic fatty liver disease. This minireview aims to discuss adipose-derived FA flux as a determinator for development of MASLD from an adipocentric perspective, underlining the contribution of WAT dysfunction in this disease.