| Abstrakt: |
A recent study conducted by researchers at the University of Southern California Keck School of Medicine has provided new insights into fatty liver disease. The study focuses on the central role of mitochondrial metabolism in hepatic steatosis, a condition characterized by the accumulation of fat in the liver. The researchers found that mitochondrial shuttles and carriers play a key role in the influx and efflux of metabolites and molecules across the inner membrane of the mitochondria. Additionally, they discovered that the interaction between a protein called SAB/SH3BP5 and c-Jun N-terminal kinase (JNK) is crucial in the activation of lipogenic pathways in nutritional excess. Knockout or knockdown of SAB was found to prevent or reverse hepatic steatosis, inflammation, and fibrosis, and improve metabolic intolerance and energy expenditure. The study highlights the importance of mitochondrial metabolism and stress signals in the development of fatty liver disease. [Extracted from the article] |
