scholarly journals Magnolia officinalis Reverses Alcoholic Fatty Liver by Inhibiting the Maturation of Sterol Regulatory Element–Binding Protein-1c

2009 ◽  
Vol 109 (4) ◽  
pp. 486-495 ◽  
Author(s):  
Hu-Quan Yin ◽  
Young-Tae Je ◽  
Young-Chul Kim ◽  
Young-Kee Shin ◽  
SangHyun Sung ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Binding Protein ◽  
Regulatory Element ◽  
Alcoholic Fatty Liver ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Magnolia Officinalis

Viral hepatitis and fatty liver disease: how an unwelcome guest makes pâté of the host

2008 ◽  
Vol 416 (2) ◽  
pp. e15-e17 ◽  
Author(s):  
Andrew J. Brown
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Regulatory Element ◽  
Alcoholic Fatty Liver ◽  
Biochemical Journal ◽  
Liver X Receptor Α ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Phosphoinositide 3 Kinase

HBV and HCV (hepatitis B and C viruses respectively) affect hundreds of millions of people globally, and are a major cause of chronic liver disease, including NAFLD (non-alcoholic fatty liver disease). Previous work on HCV-associated fatty liver disease has implicated two transcription factors that are important in lipid metabolism, SREBP1c (sterol-regulatory-element-binding protein 1c) and the LXRα (liver X receptor α). HBV-associated fatty liver disease has been less well-studied. New work from Kim and colleagues in this issue of the Biochemical Journal has provided new insight into how HBV causes fatty liver disease. Investigating HBV's so-called X gene product (HBx), they report that this viral protein directly binds to LXRα in the host liver cells to up-regulate the lipogenic transcription factor, SREBP1c. Also discussed in this commentary is another way that viruses such as HBV and HCV could induce SREBP1c-mediated lipogenesis, via the PI3K (phosphoinositide 3-kinase)–Akt signalling pathway.

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