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Branched‐chain fatty acids lower triglyceride levels in a fatty liver model in vitro
Author(s) -
Liu Lei,
Xiao Dingfu,
Lei Hongyu,
Peng Tao,
Li Jiao,
Cheng Tianyin,
He Jianhua
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.969.4
Subject(s) - triglyceride , fatty liver , oleic acid , fatty acid , chemistry , viability assay , biochemistry , palmitic acid , liver cell , albumin , cell , medicine , cholesterol , disease
Branched‐chain fatty acids (BCFA) are saturated fatty acids with one or more methyl groups. They are bioactive dietary components, and the estimated intake of BCFA in the U.S is about 500 mg/d. However, the functional role of BCFA as a nutrient has long been neglected. Non‐alcoholic fatty liver disease (NAFLD) is a hepatic metabolic syndrome characterized by the accumulation of triglycerides (TG) intracellularly. Its prevalence reaches a soaring rate, causing considerable public health concern globally. The present study aims to investigate the possible methodology of exploiting BCFA to decrease levels of TG in a fatty liver cell model. Methods L02 cells, a non‐malignant human liver cell line, were induced with oleic acids and palmitic acids at a ratio of 2:1 to establish a fatty liver model. Iso ‐15:0 (13‐methyltetradecanoic acid) and iso ‐18:0 (16‐methylheptadecanoic acid), bound to bovine serum albumin (BSA), were added to cell culture medium and co‐incubated for 24 h, respectively. TG levels were measured in cell pellets. Gene expressions of key enzymes and transcription factors involved in lipid metabolism were measured by qPCR. PPARa and SREBP‐1c were also analyzed by western‐blotting (WB). Results Co‐incubation of L02 cells with iso ‐15:0 and iso ‐18:0 ranging from 0.1 mM to 0.8 mM did not significantly hamper cell viability as shown by MTT assay. Treatment with 0.25 mM iso ‐15:0 and 0.25 mM iso ‐18:0 both significantly decreased intracellular TG content compared with fatty liver model group ( p <0.05). Gene expressions of ACOX1, CPT1, CPT2 and PPARa were enhanced by 0.25 mM iso ‐15:0 and 0.25 mM iso ‐18:0 ( p <0.05, for PPARa p <0.01). mRNA levels of SREBP‐1c and ACC were increased by 0.25 mM iso ‐15:0 (p<0.05), and mRNA levels of FASN were decreased by BCFA treatment ( p <0.05). Protein levels of PPARa and SREBP‐1c were increased upon BCFA treatment as shown by WB. Conclusion Those data indicated that BCFA could lower intracellular triglyceride content in a fatty liver model in vitro mainly by enhancing gene expressions of key enzymes in lipid catabolism via PPARa. However, the molecular mechanism needs to be illustrated in further, and the TG‐lowering effect of BCFA needs to be confirmed in vivo . Support or Funding Information Acknowledgement This work was supported by “the National Natural Science Foundation of China” (Grant No. 31502135), “the Science Fund for Distinguished Young Scholars of Education Department of Hunan Province” (Grant No. 16B124) and “Scientific Research Foundation for the introduction of talent in Hunan Agricultural University” (Grant No. 2016ZK17).