At present, there is no approved treatment for fatty liver disease (MASLD) associated with metabolic dysfunction. Albumin is a plasma protein produced by the liver, which has anti-inflammatory and antioxidant properties and is reduced in advanced liver diseases. Considering the role of inflammation induced by chronic obesity in the pathogenesis of MASLD, we studied whether albumin administration can prevent the disease from developing into steatohepatitis (MASH) related to metabolic dysfunction. Mice were treated with high fat and cholesterol (PC) for 8 weeks, and then bovine serum albumin (BSA0.8 mg/kg) was used once every three days for 8 weeks. This scheme prevented the time-dependent weight gain unrelated to diet, which was reduced by 57% and 27% in mice fed with standard food (Std food) or PC food, respectively. In addition, in PC-fed mice, the supplement reduced the activation of nuclear factor κB(NF-κB) by 2.8 times (p = 0.0328), which is consistent with the known anti-inflammatory properties of albumin. Unexpectedly, albumin also reduced the accumulation of neutral lipids in the liver and non-esterified fatty acids in the circulation. Although PC-fed mice did not show complete progress to MASH, albumin treatment significantly increased the expression of matrix metalloproteinase -2 in liver, indicating the inhibition of early fibrosis signals. Although further research is needed to clarify the underlying mechanism, these findings provide a new insight into the potential of albumin alone or in combination with other therapies to reduce hepatic steatosis in patients with MASLD.

At present, there is no approved treatment for fatty liver disease (MASLD) associated with metabolic dysfunction. Albumin is a plasma protein produced by the liver, which has anti-inflammatory and antioxidant properties and is reduced in advanced liver diseases. Considering the role of inflammation induced by chronic obesity in the pathogenesis of MASLD, we studied whether albumin administration can prevent the disease from developing into steatohepatitis (MASH) related to metabolic dysfunction. Mice were treated with high fat and cholesterol (PC) for 8 weeks, and then bovine serum albumin (BSA0.8 mg/kg) was used once every three days for 8 weeks. This scheme prevented the time-dependent weight gain unrelated to diet, which was reduced by 57% and 27% in mice fed with standard food (Std food) or PC food, respectively. In addition, in PC-fed mice, the supplement reduced the activation of nuclear factor κB(NF-κB) by 2.8 times (p = 0.0328), which is consistent with the known anti-inflammatory properties of albumin. Unexpectedly, albumin also reduced the accumulation of neutral lipids in the liver and non-esterified fatty acids in the circulation. Although PC-fed mice did not show complete progress to MASH, albumin treatment significantly increased the expression of matrix metalloproteinase -2 in liver, indicating the inhibition of early fibrosis signals. Although further research is needed to clarify the underlying mechanism, these findings provide a new insight into the potential of albumin alone or in combination with other therapies to reduce hepatic steatosis in patients with MASLD.