Effects of 5-iodotubercidin on hepatic fatty acid metabolism mediated by the inhibition of acetyl-CoA carboxylase

2002 ◽  
Vol 63 (11) ◽  
pp. 1997-2000 ◽  
Author(s):  
Javier Garcı́a-Villafranca ◽  
José Castro
2020 ◽  
Author(s):  
Ada Admin ◽  
Zhuo Mao ◽  
Mingji Feng ◽  
Zhuoran Li ◽  
Minsi Zhou ◽  
...  

ETV5 is an ETS transcription factor which has been associated with obesity in genomic association studies. However, little is known about the role of ETV5 in hepatic lipid metabolism and non-alcoholic fatty liver disease (NAFLD). In the present study, we found that ETV5 protein expression was increased in diet- and genetic-induced steatotic liver. ETV5 responded to the nutrient status in an mTORC1 dependent manner and in turn regulated mTORC1 activity. Both viral-mediated and genetic depletion of ETV5 in mice led to increased lipid accumulation in the liver. RNA sequencing analysis revealed that PPAR signaling and fatty acid degradation/metabolism pathways were significantly downregulated in ETV5 deficient hepatocytes <i>in vivo</i> and <i>in vitro. </i>Mechanistically, ETV5 could bind to the PPRE region of PPAR downstream genes and enhance its transactivity. Collectively, our study identifies ETV5 as a novel transcription factor for the regulation of hepatic fatty acid metabolism which is required for the optimal β oxidation process. ETV5 may provide a therapeutic target for the treatment of hepatic steatosis.<br>


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Hua Yang ◽  
Fei Wang ◽  
Xinya Guo ◽  
Feng Liu ◽  
Zhonghua Liu ◽  
...  

AbstractPathogenic mycobacteria induce the formation of hypoxic granulomas during latent tuberculosis (TB) infection, in which the immune system contains, but fails to eliminate the mycobacteria. Fatty acid metabolism-related genes are relatively overrepresented in the mycobacterial genome and mycobacteria favor host-derived fatty acids as nutrient sources. However, whether and how mycobacteria modulate host fatty acid metabolism to drive granuloma progression remains unknown. Here, we report that mycobacteria under hypoxia markedly secrete the protein Rv0859/MMAR_4677 (Fatty-acid degradation A, FadA), which is also enriched in tuberculous granulomas. FadA acts as an acetyltransferase that converts host acetyl-CoA to acetoacetyl-CoA. The reduced acetyl-CoA level suppresses H3K9Ac-mediated expression of the host proinflammatory cytokine Il6, thus promoting granuloma progression. Moreover, supplementation of acetate increases the level of acetyl-CoA and inhibits the formation of granulomas. Our findings suggest an unexpected mechanism of a hypoxia-induced mycobacterial protein suppressing host immunity via modulation of host fatty acid metabolism and raise the possibility of a novel therapeutic strategy for TB infection.


2012 ◽  
Vol 52 (3) ◽  
pp. 1015-1027 ◽  
Author(s):  
Takashi Ide ◽  
Ayana Azechi ◽  
Sayaka Kitade ◽  
Yoko Kunimatsu ◽  
Natsuko Suzuki ◽  
...  

Obesity ◽  
2014 ◽  
Vol 22 (7) ◽  
pp. 1685-1693 ◽  
Author(s):  
Lisa M. Nicholas ◽  
Leewen Rattanatray ◽  
Janna L. Morrison ◽  
David O. Kleemann ◽  
Simon K. Walker ◽  
...  

1995 ◽  
Vol 227 (3) ◽  
pp. 715-722 ◽  
Author(s):  
Daniel K. Asiedu ◽  
Ayman Al-Shurbaji ◽  
Arild C. Rustan ◽  
Ingemar Bjorkhem ◽  
Lars Berglund ◽  
...  

Author(s):  
Jolita Ciapaite ◽  
Nicole M. van den Broek ◽  
Heleen te Brinke ◽  
Klaas Nicolay ◽  
Jeroen A. Jeneson ◽  
...  

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