Protective role of soluble receptor for advanced glycation end-products in patients with non-alcoholic fatty liver disease

2017 ◽  
Vol 49 (5) ◽  
pp. 523-529 ◽  
Author(s):  
Shira Zelber-Sagi ◽  
Federico Salomone ◽  
Ilana Kolodkin-Gal ◽  
Noam Erez ◽  
Assaf Buch ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver Disease ◽  
Protective Role ◽  
Soluble Receptor ◽  
Advanced Glycation ◽  
Alcoholic Fatty Liver ◽  
Glycation End Products ◽  
End Products ◽  
Alcoholic Fatty Liver Disease

scholarly journals Development and Progression of Non-Alcoholic Fatty Liver Disease: The Role of Advanced Glycation End Products

2019 ◽  
Vol 20 (20) ◽  
pp. 5037 ◽  
Author(s):  
Dinali H. Fernando ◽  
Josephine M. Forbes ◽  
Peter W. Angus ◽  
Chandana B. Herath
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Advanced Glycation ◽  
Alcoholic Fatty Liver ◽  
Second Hit ◽  
Glycation End Products ◽  
End Products ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) affects up to 30% of the adult population and is now a major cause of liver disease-related premature illness and deaths in the world. Treatment is largely based on lifestyle modification, which is difficult to achieve in most patients. Progression of simple fatty liver or steatosis to its severe form non-alcoholic steatohepatitis (NASH) and liver fibrosis has been explained by a ‘two-hit hypothesis’. Whilst simple steatosis is considered the first hit, its transformation to NASH may be driven by a second hit. Of several factors that constitute the second hit, advanced glycation end products (AGEs), which are formed when reducing-sugars react with proteins or lipids, have been implicated as major candidates that drive steatosis to NASH via the receptor for AGEs (RAGE). Both endogenous and processed food-derived (exogenous) AGEs can activate RAGE, mainly present on Kupffer cells and hepatic stellate cells, thus propagating NAFLD progression. This review focuses on the pathophysiology of NAFLD with special emphasis on the role of food-derived AGEs in NAFLD progression to NASH and liver fibrosis. Moreover, the effect of dietary manipulation to reduce AGE content in food or the therapies targeting AGE/RAGE pathway on disease progression is also discussed.

scholarly journals Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease

2016 ◽  
Vol 22 (35) ◽  
pp. 8026 ◽  
Author(s):  
Christopher Leung ◽  
Chandana B Herath ◽  
Zhiyuan Jia ◽  
Sof Andrikopoulos ◽  
Bronwyn E Brown ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Advanced Glycation End Products ◽  
Fatty Liver Disease ◽  
Advanced Glycation ◽  
Alcoholic Fatty Liver ◽  
Glycation End Products ◽  
End Products ◽  
Alcoholic Fatty Liver Disease

scholarly journals Hepatic microvascular dysfunction and increased advanced glycation end products are components of non-alcoholic fatty liver disease

PLoS ONE ◽  
2017 ◽  
Vol 12 (6) ◽  
pp. e0179654 ◽  
Author(s):  
Evelyn Nunes Goulart da Silva Pereira ◽  
Raquel Rangel Silvares ◽  
Edgar Eduardo Ilaquita Flores ◽  
Karine Lino Rodrigues ◽  
Isalira Peroba Ramos ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Advanced Glycation End Products ◽  
Fatty Liver Disease ◽  
Microvascular Dysfunction ◽  
Advanced Glycation ◽  
Alcoholic Fatty Liver ◽  
Glycation End Products ◽  
End Products ◽  
Alcoholic Fatty Liver Disease

Protective Role of Coffee in Non-alcoholic Fatty Liver Disease (NAFLD)

2010 ◽  
Vol 55 (11) ◽  
pp. 3200-3206 ◽  
Author(s):  
Daniela Catalano ◽  
Giuseppe Fabio Martines ◽  
Antonia Tonzuso ◽  
Clara Pirri ◽  
Francesca M. Trovato ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Protective Role ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease
Sign in / Sign up

Export Citation Format

Share Document