Details

Autor(en) / Beteiligte

• Lim, Andrea
• Zhou, Jin
• Sinha, Rohit A.
• Singh, Brijesh K.
• Ghosh, Sujoy
• Lim, Kiat-Hon
• Chow, Pierce Kah-Hoe
• Woon, Esther C.Y.
• Yen, Paul M.

Titel

Hepatic FTO expression is increased in NASH and its silencing attenuates palmitic acid-induced lipotoxicity

Ist Teil von

• Biochemical and biophysical research communications, 2016-10, Vol.479 (3), p.476-481

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2016

Quelle

MEDLINE

Beschreibungen/Notizen

• Non-alcoholic steatohepatitis (NASH) is one of the most common causes of liver failure worldwide. It is characterized by excess fat accumulation, inflammation, and increased lipotoxicity in hepatocytes. Currently, there are limited treatment options for NASH due to lack of understanding of its molecular etiology. In the present study, we demonstrate that the expression of fat mass and obesity associated gene (FTO) is significantly increased in the livers of NASH patients and in a rodent model of NASH. Furthermore, using human hepatic cells, we show that genetic silencing of FTO protects against palmitate-induced oxidative stress, mitochondrial dysfunction, ER stress, and apoptosis in vitro. Taken together, our results show that FTO may have a deleterious role in hepatic cells during lipotoxic conditions, and strongly suggest that up-regulation of FTO may contribute to the increased liver damage in NASH. •FTO expression is increased in NASH patients and rodent models of NASH.•Silencing of FTO protects against PA-induced ER-stress and apoptosis.•Silencing of FTO attenuates palmitate-induced mitochondrial dysfunction.