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

Leung, Christopher, Herath, Chandana B., Jia, Zhiyuan, Andrikopoulos, Sof, Brown, Bronwyn E., Davies, Michael J., Rivera, Leni R., Furness, John B., Forbes, Josephine M. and Angus, Peter W. 2016, Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease, World journal of gastroenterology, vol. 22, no. 35, pp. 8026-8040, doi: 10.3748/wjg.v22.i35.8026.

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Title Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease
Author(s) Leung, Christopher
Herath, Chandana B.
Jia, Zhiyuan
Andrikopoulos, Sof
Brown, Bronwyn E.
Davies, Michael J.
Rivera, Leni R.
Furness, John B.
Forbes, Josephine M.
Angus, Peter W.
Journal name World journal of gastroenterology
Volume number 22
Issue number 35
Start page 8026
End page 8040
Total pages 15
Publisher Baishideng Publishing Group
Place of publication Pleasanton, Calif.
Publication date 2016-09-21
ISSN 1007-9327
2219-2840
Keyword(s) advanced glycation end-products
fructose
hepatic fibrosis
non-alcoholic fatty liver disease
oxidative stress
steatohepatitis
Summary AIM: To determine if manipulation of dietary advanced glycation end product (AGE), intake affects non-alcoholic fatty liver disease (NAFLD) progression and whether these effects are mediated via RAGE. METHODS: Male C57Bl6 mice were fed a high fat, high fructose, high cholesterol (HFHC) diet for 33 wk and compared with animals on normal chow. A third group were given a HFHC diet that was high in AGEs. Another group was given a HFHC diet that was marinated in vinegar to prevent the formation of AGEs. In a second experiment, RAGE KO animals were fed a HFHC diet or a high AGE HFHC diet and compared with wildtype controls. Hepatic biochemistry, histology, picrosirius red morphometry and hepatic mRNA were determined. RESULTS: Long-term consumption of the HFHC diet generated significant steatohepatitis and fibrosis after 33 wk. In this model, hepatic 4-hydroxynonenal content (a marker of chronic oxidative stress), hepatocyte ballooning, picrosirius red staining, α-smooth muscle actin and collagen type 1A gene expression were all significantly increased. Increasing the AGE content of the HFHC diet by baking further increased these markers of liver damage, but this was abrogated by pre-marination in acetic acid. In response to the HFHC diet, RAGE(-/-) animals developed NASH of similar severity to RAGE(+/+) animals but were protected from the additional harmful effects of the high AGE containing diet. Studies in isolated Kupffer cells showed that AGEs increase cell proliferation and oxidative stress, providing a likely mechanism through which these compounds contribute to liver injury. CONCLUSION: In the HFHC model of NAFLD, manipulation of dietary AGEs modulates liver injury, inflammation, and liver fibrosis via a RAGE dependent pathway. This suggests that pharmacological and dietary strategies targeting the AGE/RAGE pathway could slow the progression of NAFLD.
Language eng
DOI 10.3748/wjg.v22.i35.8026
Field of Research 111103 Nutritional Physiology
1103 Clinical Sciences
Socio Economic Objective 920411 Nutrition
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2016, Baishideng Publishing Group
Free to Read? Yes
Use Rights Creative Commons Attribution non-commercial licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30091794

Document type: Journal Article
Collections: School of Medicine
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.