NDLI: Impact of activating transcription factor 4 signaling on lipogenesis in HepG2 cells.

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Impact of activating transcription factor 4 signaling on lipogenesis in HepG2 cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Xue-Mei Chen, Shu-Chun Song, Guang-Yao Sun, Li-Na Yu, Xian Ren, Lu-Ping Hu, Zhi-Juan Zhang, Pu
Description	Author Affiliation: Ren LP ( Department of Endocrinology and Metabolism, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.); Yu X ( Department of Endocrinology and Metabolism, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.); Song GY ( Department of Endocrinology and Metabolism, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.); Zhang P ( Department of Endocrinology and Metabolism, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.); Sun LN ( Department of Endocrinology and Metabolism, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.); Chen SC ( Department of Endocrinology and Metabolism, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.); Hu ZJ ( Department of Nephrology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.); Zhang XM ( Department of Endocrinology and Metabolism, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.)
Abstract	Non-alcoholic fatty liver disease (NAFLD) is a rapidly growing health threat that has previously been associated with lipogenesis. The direct effect of endoplasmic reticulum stress (ERS) inhibition on the induction of lipogenesis has not been investigated in hepatocytes in vitro. The impact of activating transcription factor4 (ATF4) on the lipogenic pathway and hepatic insulin transduction in liver cells also requires further investigation. In the present study, the triglyceride (TG) content of HepG2 cells stimulated with fructose was investigated using a commercially available enzymatic assay, and the expression levels of lipogenesisassociated factors were determined by western blotting and reverse transcriptionquantitative polymerase chain reaction. Notably, the TG content of HepG2 cells was increased following incubation with fructose, which was accompanied by ERS. 4Phenylbutyric acid, an inhibitor of ERS, lowered the TG content by reducing the mRNA expression levels of sterol regulatory elementbinding protein 1 (SREBP1c) and carbohydrateresponsive elementbinding protein (ChREBP), and the protein expression levels of fatty acid synthase (FAS), acetylCoA carboxylase (ACC) and stearoylCoA desaturase1 (SCD1). Conversely, tunicamycin, which is an inducer of ERS, increased the TG content and stimulated the expression of the above lipogeneic markers. ATF4 deficiency relieved TG accumulation and decreased the mRNA expression levels of SREBP1c and ChREBP, and protein expression levels of FAS, ACC and SCD1 in fructosetreated HepG2 cells. Conversely, ATF4 overexpression increased the TG content by upregulating the mRNA expression levels of SREBP1c and ChREBP and protein expression levels of FAS, ACC and SCD1. Inhibition of ERS was shown to protect HepG2 cells against fructoseinduced TG accumulation, whereas induction of ERS stimulated hepatic lipogenesis. As a downstream transcription factor of the unfolded protein response, a deficiency in ATF4 attenuates fructoseinduced lipogenesis; while an overexpression of ATF4 can induce TG accumulation through stimulating hepatic lipogenesis. The results of the present study suggested that ATF4 may exert various physiological roles in lipid metabolism depending on the nutrient composition. In addition, these results suggested that ATF4 has a role in regulating lipogenesis and in the development of NAFLD; thus ATF4 may be considered a therapeutic target for NAFLD.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	2
Volume Number	14
Language	English
Publisher	Spandidos Publications
Publisher Date	2016-08-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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