Sodium butyrate alleviates fructose-induced non-alcoholic fatty liver disease by remodeling gut microbiota to promote γ-amino butyric acid production
文献类型： 外文期刊
作者： Chen, Qu 1 ; Wu, Lei 1 ; Zhang, Aijia 1 ; Wu, Chen 1 ; Cai, Liuping 1 ; Xiao, Yingping 2 ; Ni, Yingdong 1 ;
作者机构： 1.Nanjing Agr Univ, Minist Agr & Rural Affairs, Key Lab Anim Physiol & Biochem, Nanjing, Peoples R China
2.Zhejiang Acad Agr Sci, Inst Agroprod Safety & Nutr, State Key Lab Managing Biot & Chem Threats Qual &, Hangzhou 310021, Peoples R China
关键词： Butyrate; Fructose; Gut microbiota; Hepatic steatosis
期刊名称：FOOD SCIENCE AND HUMAN WELLNESS （ 影响因子：7.0； 五年影响因子：8.3 ）
ISSN：
年卷期： 2024 年 13 卷 2 期
页码：
收录情况： SCI
摘要： Sodium butyrate (NaB) can regulate lipid metabolism and inhibit hepatic steatosis. This study aimed to investigate whether NaB can alleviate fructose-induced hepat ic steatosis via remodeling the gut microbiota and evaluate the anti-fatty liver mechanisms. The results showed that NaB and NaB-remodeled gut microbiota significantly alleviated fructose-induced hepatic steatosis and increased plasma uric acid and fructose levels. Furthermore, both NaB and NaB-remodeled gut microbiota increased the abundance of Lactobacillus and altered the levels of plasma amino acids (upregulating gamma-amino butyric acid (GABA) and downregulating L-glutamic acid and L-arginine) in fructose-exposed mice. The correlation analysis showed that GABA levels positively correlated with Lactobacillus abundance, and increased GABA levels might promote the reduction of the hepatic triglyceride content. Further studies confirmed that GABA significantly reduced lipid deposition in mouse hepatocytes induced via fructose pretreatment in vitro. These findings suggested that NaB could ameliorate fructose-induced hepatic steatosis by regulating gut microbiota.(c) 2024 Beijing Academy of Food Sciences. Publishing services by Tsinghua University Press. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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