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

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

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.; Angus, Peter W.

In: World Journal of Gastroenterology, Vol. 22, No. 35, 21.09.2016, p. 8026-8040.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Leung, C, Herath, CB, Jia, Z, Andrikopoulos, S, Brown, BE, Davies, MJ, Rivera, LR, Furness, JB, Forbes, JM & Angus, PW 2016, 'Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease', World Journal of Gastroenterology, vol. 22, no. 35, pp. 8026-8040. https://doi.org/10.3748/wjg.v22.i35.8026

APA

Leung, C., Herath, C. B., Jia, Z., Andrikopoulos, S., Brown, B. E., Davies, M. J., ... Angus, P. W. (2016). Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease. World Journal of Gastroenterology, 22(35), 8026-8040. https://doi.org/10.3748/wjg.v22.i35.8026

Vancouver

Leung C, Herath CB, Jia Z, Andrikopoulos S, Brown BE, Davies MJ et al. Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease. World Journal of Gastroenterology. 2016 Sep 21;22(35):8026-8040. https://doi.org/10.3748/wjg.v22.i35.8026

Author

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. / Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease. In: World Journal of Gastroenterology. 2016 ; Vol. 22, No. 35. pp. 8026-8040.

Bibtex

@article{15fbe2487cc34a68918f98fe0e71008d,
title = "Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease",
abstract = "AIM To determine if manipulation of dietary advanced glycation end product (AGE), intake affects nonalcoholic 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.",
keywords = "Advanced glycation end-products, Fructose, Hepatic fibrosis, Non-alcoholic fatty liver disease, Oxidative stress, Steatohepatitis",
author = "Christopher Leung and Herath, {Chandana B.} and Zhiyuan Jia and Sof Andrikopoulos and Brown, {Bronwyn E.} and Davies, {Michael J.} and Rivera, {Leni R.} and Furness, {John B.} and Forbes, {Josephine M.} and Angus, {Peter W.}",
year = "2016",
month = "9",
day = "21",
doi = "10.3748/wjg.v22.i35.8026",
language = "English",
volume = "22",
pages = "8026--8040",
journal = "World Journal of Gastroenterology",
issn = "1007-9327",
publisher = "Baishideng Publishing Group Co., Limited",
number = "35",

}

RIS

TY - JOUR

T1 - Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease

AU - Leung, Christopher

AU - Herath, Chandana B.

AU - Jia, Zhiyuan

AU - Andrikopoulos, Sof

AU - Brown, Bronwyn E.

AU - Davies, Michael J.

AU - Rivera, Leni R.

AU - Furness, John B.

AU - Forbes, Josephine M.

AU - Angus, Peter W.

PY - 2016/9/21

Y1 - 2016/9/21

N2 - AIM To determine if manipulation of dietary advanced glycation end product (AGE), intake affects nonalcoholic 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.

AB - AIM To determine if manipulation of dietary advanced glycation end product (AGE), intake affects nonalcoholic 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.

KW - Advanced glycation end-products

KW - Fructose

KW - Hepatic fibrosis

KW - Non-alcoholic fatty liver disease

KW - Oxidative stress

KW - Steatohepatitis

UR - http://www.scopus.com/inward/record.url?scp=84991086703&partnerID=8YFLogxK

U2 - 10.3748/wjg.v22.i35.8026

DO - 10.3748/wjg.v22.i35.8026

M3 - Journal article

VL - 22

SP - 8026

EP - 8040

JO - World Journal of Gastroenterology

JF - World Journal of Gastroenterology

SN - 1007-9327

IS - 35

ER -

ID: 210609363