To reveal the potential treatment strategies of nonalcoholic fatty liver disease in obese people
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Nonalcoholic fatty liver disease (NAFLD) is a very common disease, which is characterized by elevated triglyceride content in the liver, not due to excessive drinking. Nonalcoholic fatty liver disease is usually asymptomatic in the early stage, but if not treated, it will lead to a series of advanced metabolism and liver diseases, such as cirrhosis and cancer.
Obesity, type 2 diabetes and dyslipidemia are recognized risk factors for NAFLD. In addition, conditions that cause dysregulation of liver methionine metabolism, such as rapid weight loss, hunger and malnutrition, may also lead to NAFLD.
Recently, researchers from the University of Hong Kong published in the Journal theranostics entitled “hepatic PRMT1 ameliorites die induced hepatic stearosis via induction of PGC1” α” The results show that PRMT1 / HNF-4 is activated α/ pGC-1 α Signaling pathway is a potential therapeutic strategy against nonalcoholic fatty liver disease in obese people.
图片来源: https://pubmed.ncbi.nlm.nih.gov/35401831/
Over nutrition leads to overexpression of PRMT1, but hypomethylation of protein is observed in the liver of obese people. The dynamic changes of PRMT1 expression and methyltransferase activity in the progression of fatty liver disease remain elusive.
In this study, the researchers used the recombinant adeno-associated virus mediated gene delivery system to regulate the expression level of PRMT1 in the liver of diet induced obese mice, so as to explore the role of PRMT1 in liver steatosis. The researchers further used a group of obese people with biopsy confirmed nonalcoholic fatty liver disease to support the observation in mouse models.
The researchers demonstrated that the knockout of PRMT1 gene promoted the occurrence of hepatic steatosis in high-fat diet (HFD) mice. Overexpression of wild-type PRMT1, rather than methyltransferase deficient mutant prmt1g80r, can reduce diet induced hepatic steatosis. This observation is conservative in a sample of obese people with biopsy confirmed nonalcoholic fatty liver disease.
In terms of mechanism, the methyltransferase activity of PRMT1 α- four α Raised to PGC-1 α To induce PGC-1 α To reduce hepatic steatosis induced by HFD by enhancing pgc-1-mediated fatty acid oxidation.
Liver PRMT1 induces PGC1 α Improve feed induced hepatic steatosis
图片来源: https://pubmed.ncbi.nlm.nih.gov/35401831/
To sum up, the researchers passed HNF-4 α And PGC-1 α The mechanism dependent induction of hepatic fatty acid oxidation reveals the protective effect of PRMT1 on hepatic steatosis in obese subjects. The findings of this study help explain why methyl donor supplementation prevented the progression of NAFLD in obese subjects. PRMT1 inhibitors are being developed to treat various cancers, so it is necessary to evaluate the potential side effects of PRMT1 inhibitor treatment on liver lipid metabolism and liver injury.
reference:
Lu Xu et al. Hepatic PRMT1 ameliorates diet-induced hepatic steatosis via induction of PGC1α. Theranostics. 2022 Feb 28;12(6):2502-2518. doi: 10.7150/thno.63824.
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