Researchers at the Stowers Institute for Medical Research have identified a gene named slc27a2a that appears to shield the fat metabolism process of the fish species Astyanax mexicanus from fatty liver disease. The findings, published in Life Science Alliance (LSA), suggest that this gene plays a protective role in hepatic lipid regulation under certain conditions.
In humans, the leading causes of fatty liver disease include poor nutrition, alcohol consumption, certain medications, and metabolic syndrome, which encompasses obesity and diabetes. Fatty liver disease involves the buildup of lipid-like substances inside liver tissue. This accumulation can arise from both excess food intake and periods of fasting, illustrating the liver’s sensitivity to changes in energy balance.
Studies on Astyanax mexicanus revealed that individuals within this species exhibit reduced expression of slc27a2a. This freshwater ray-finned fish belongs to the characin family and is native to the Americas and Mexico. Notably, the species lacks eyes and pigmentation. The research shows that lowered slc27a2a activity corresponds with a broader tolerance to energy scarcity and a reduced propensity for hepatic fat accumulation, enabling the fish to better withstand episodes of food deprivation without triggering harmful lipid buildup in the liver.
Fat droplets accumulating in liver cells are associated with cellular injury and an elevated risk of progressing to cirrhosis, a condition characterized by scar tissue proliferation and compromised liver function. The scientists propose that decreasing slc27a2a activity could, in humans, potentially mitigate the damaging effects of lipids on liver tissue. However, they caution that further research is necessary to determine whether this mechanism can be translated into practical therapies for people and to understand the broader implications for human liver health.
Earlier milestones include the approval of a first-ever medication targeting fatty liver disease in the United States, marking a significant step in clinical management of the condition. The current findings underscore the value of cross-species analyses for uncovering genetic pathways that influence lipid handling in the liver and highlight the ongoing scientific exploration needed to translate such insights into effective treatments for human patients.