On August 11, Hainan University announced a significant discovery by Prof. Huang Ling’s team from the School of Pharmaceutical Sciences. The team found that L-aspartic acid can reverse the mitochondrial metabolic impairment caused by liver metabolic disorders. The finding has been published in the international academic journal Pharmacological Research.

During the liver’s healing process, excessive proliferation of fibrous tissue can lead to liver fibrosis. This condition occurs in the late stage of chronic liver diseases and, if left unchecked, may progress to cirrhosis or even liver cancer. In recent years, the incidence of liver fibrosis has been on the rise. However, there are currently few drugs available for targeted therapies, underscoring the urgency of new drug development.

 “Amino acid metabolism disorders can cause disruptions in the metabolism of glucose, lipids, and bile acids in the liver, leading to mitochondrial dysfunction and, subsequently, liver disease,” explained Prof. Huang. Based on research into amino acid metabolism in the liver, the search for endogenous active substances with hepatoprotective and anti-fibrotic properties —along with clarifying their physiological and pharmacological mechanisms—represents a new frontier in the R&D of innovative drugs for liver diseases.

In earlier studies, Huang’s team used non-targeted metabolomics to identify, for the first time, that metabolic disorders related to the liver-gut axis, particularly L-aspartic acid metabolism, are a key factor in the development of metabolic dysfunction-associated fatty liver disease (MAFLD). The team further observed that oral administration of L-aspartic acid in mice effectively reversed carbon tetrachloride-induced acute liver injury and fibrosis.

According to the outcome, the team concludes that L-aspartic acid can regulate the metabolic balance of cholesterol and steroids in the liver, prevent the excessive accumulation of corticosterone, and inhibit its activation of glucocorticoid receptors. This, in turn, restores mitochondrial metabolic function, thereby protecting the liver.

Source from Science and Technology Daily

Translated by Han Yunsheng

Proofread by Kuang Xiaowen, Yang Jie