Recently, the international academic journal The Journal of Lipid Research published online the research paper Liver Patt1 deficiency protects male mice from Age-associated but not high-fat diet-induced hepatic steatosis of the Research Group of the Institute of Nutrition, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences. In this study, liver-specific knockout of acetylase Patt1 (Protein acetyltransferase-1) mice was used as a model to discover the important role and related mechanism of acetylase Patt1 in liver lipid metabolism.
Nonalcoholic fatty liver disease (nonalcoholic fatty liver disease) is a clinical pathological syndrome characterized by no history of excessive drinking, hepatic parenchymal cell steatosis and fat storage. Its main risk factors include age, obesity, type 2 diabetes Hyperlipidemia, etc. Liver steatosis is an early state of non-alcoholic fatty liver, and its occurrence is also related to the above factors. Liver steatosis is caused by excessive accumulation of triglycerides in liver cells, and its formation mechanism includes increased fatty acid intake, increased fat synthesis, decreased fatty acid oxidation and / or decreased liver fat output. However, the detailed molecular mechanism of liver steatosis remains to be studied.
Patt1 is a protein acetylase highly expressed in liver tissue identified and named by Zhai Qiwei's research group. Its biological function in the liver is not yet clear. In order to study the function of Patt1 in the liver, PhD student Liu Yang and others constructed liver-specific knockout mice. The study found that liver Patt1 knockout mainly had a significant effect on lipid metabolism in male mice. The specific performance is that the body fat content of mice is significantly reduced, and the accumulation of age-related liver lipid droplets is also significantly reduced; the content of triglycerides and free fatty acids in the liver is reduced, but cholesterol, liver weight and liver function have not changed significantly. Hepatocyte-specific Patt1 knockout can alleviate fatty acid-induced accumulation of lipid droplets in primary liver cells of mice, but liver Patt1 knockout has no resistance to fatty liver induced by high-fat diet in mice.
Further research found that liver Patt1 knockout can reduce liver fatty acid intake, reduce fat synthesis, and enhance fatty acid oxidation, which can lead to a significant reduction in liver fat accumulation.
The above results show that Patt1 plays an important role in liver lipid metabolism, which provides new clues for the in-depth understanding of the pathogenesis of liver steatosis, and also provides a potential new target for the treatment of age-related liver steatosis.
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