Effect of Dibutyltin Dilaurate on Triglyceride Metabolism through the Inhibition of the mTOR Pathway in Human HL7702 Liver Cells

• Published in: Molecules (Basel, Switzerland) Vol. 23; no. 7; p. 1654
• Main Authors: Qiao, Xiaozhi, Li, Yunlan, Mai, Jiaqi, Ji, Xiaoqing, Li, Qingshan
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 06-07-2018; MDPI
• Subjects: Cell Line; Cell Survival - drug effects; dibutyltin dilaurate (DBTD); Dose-Response Relationship, Drug; Gene expression; Gene Expression Regulation - drug effects; Genes; Hepatocytes; Hepatocytes - cytology; Hepatocytes - drug effects; Hepatocytes - metabolism; Humans; Intracellular; Kinases; Lipid Metabolism - drug effects; Lipogenesis; Lipolysis; Liver; Metabolism; mTOR pathway; Organotin Compounds - pharmacology; Phosphorylation; Phosphorylation - drug effects; PPAR alpha - genetics; PPARα; Proteins; Rapamycin; Ribosomal protein S6 kinase; Ribosomal Protein S6 Kinases, 70-kDa - metabolism; Signal Transduction - drug effects; Sirolimus - pharmacology; SREBP1C; Sterol Regulatory Element Binding Protein 1 - genetics; Sterol regulatory element-binding protein; Sterol regulatory element-binding protein 1c; TOR protein; TOR Serine-Threonine Kinases - metabolism; Transcription factors; Triglycerides - metabolism; SREBP1C; mTOR pathway; triglycerides metabolism; dibutyltin dilaurate (DBTD); PPARα
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules23071654

Dibutyltin dilaurate (DBTD) has multiple applications in daily life. However, DBTD is easily deposited in the liver and affects liver functions. This study was designed to explore the effects of DBTD on triglyceride metabolism in human normal hepatocyte HL7702 cells. Our results showed that the intracellular fat contents were dose-dependently decreased by DBTD. The expression of lipolysis genes and proteins were elevated while the lipogenesis genes and proteins were diminished by DBTD. The phosphorylation levels of ribosomal S6 kinase 1 were reduced by both rapamycin and DBTD, indicating that the mTOR pathway was suppressed possibly. The decreased sterol regulatory element-binding protein 1C (SREBP1C) transcription levels, as well as the increased peroxisome proliferator-activated receptor alpha (PPARα) transcription levels, caused by rapamycin and DBTD corresponded to the inactive mTOR pathway. In conclusion, it was possible that DBTD reduced the intracellular triglyceride through depressing the mTOR pathway and affecting its downstream transcription factors.