Page 76 - ebook

[A. Biochemistry/Molecular Biology] A-38

Sodium Butyrate increases hepatic lipid accumulation

Hyun Jae Sung¹, Dong Yeol Kim¹, Jiwon Park¹, Sang-Min Kim¹, Quynh Nguyen Thi Nhu¹, Duong Tran Thi

Thuy¹, An Bui Ngan¹, Inn-Oc Han¹*

¹Biomedical Science and Engineering, Inha university, Incheon 22212, Korea

Short Chain Fatty Acids (SCFAs) including butyrate are produced from dietary fiber by gut microbiota. Butyrate has

been shown that reduce lipid accumulation in human hepatocytes in high fat conditions. However, it still remains

unclear the mechanism by which butyrate regulates hepatic lipid accumulation. In the current study, we newly
discovered that sodium butyrate (NaB) induces lipid accumulation in Hep G2 cells in dose dependent manner under
normal glucose conditions. Other types of SCFA such as acetate or propionate did not induce lipid accumulation in

Hep G2 cells. Since NaB is a histone deacetylase (HDAC) inhibitor, we examined the effect of another well known
HDAC inhibitor, Trichostatin A (TSA) for lipid accumulation in Hep G2 cells. TSA also induced lipid accumulation in

Hep G2 cells in dose dependent manner. NaB resulted in lipid accumulation in the liver of zebrafish under the
normal diet condition. Both NaB and TSA increased protein and mRNA expression of sterol regulatory element-

binding protein 1c (SREBP-1c) and fatty acid synthase (FAS), a key markers related to fat accumulation, in Hep G2
cells in a dose dependent manner. Our study collectively indicates that NaB increased hepatic lipid accumulation

under normal diet conditions potentially through HDAC pathway