Dietary glycotoxins exacerbate progression of experimental fatty liver disease

Leung, Christopher; Herath, Chandana B; Jia, Zhiyuan; Goodwin, Michelle; Mak, Kai Yan; Watt, Matthew James; Forbes, Josephine M.; Angus, Peter W

doi:10.1016/j.jhep.2013.11.033

Cited by 77 publications

(74 citation statements)

References 37 publications

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“…The study by Leung and coworkers [62] compared the expression of RAGE in three groups of animals fed with diets in pelletized form: one fed with a standard diet, another with a CMD (cysteine/methionine deficient) diet, and finally a group that was fed with a CMD diet prepared with additional heating. One of the results observed was an increase in these receptors (RAGE) in the third group, most likely due to the higher amount of exogenous AGEs ingested [62].…”

Section: Discussionmentioning

confidence: 99%

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Choline and Cystine Deficient Diets in Animal Models with Hepatocellular Injury: Evaluation of Oxidative Stress and Expression of RAGE, TNF-α, and IL-1β

Santos

Araújo

Valentim

et al. 2015

Oxidative Medicine and Cellular Longevity

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This study aims to evaluate the effects of diets deficient in choline and/or cystine on hepatocellular injury in animal models (young male Wistar rats, aged 21 days), by monitoring some of the oxidative stress biomarkers and the expression of RAGE, TNF-α, and IL-1β. The animals were divided into 6 groups (n = 10) and submitted to different diets over 30 days: AIN-93 diet (standard, St), AIN-93 choline deficient (CD) diet and AIN-93 choline and cystine deficient (CCD) diet, in the pellet (pl) and powder (pw) diet forms. Independently of the diet form, AIN-93 diet already led to hepatic steatosis and CD/CCD diets provoked hepatic damage. The increase of lipid peroxidation, represented by the evaluation of thiobarbituric acid reactive species, associated with the decrease of levels of antioxidant enzymes, were the parameters with higher significance toward redox profile in this model of hepatic injury. Regarding inflammation, in relation to TNF-α, higher levels were evidenced in CD(pl), while, for IL-1β, no significant alteration was detected. RAGE expression was practically the same in all groups, with exception of CCD(pw) versus CCD(pl). These results together confirm that AIN-93 causes hepatic steatosis and choline and/or cysteine deficiencies produce important hepatic injury associated with oxidative stress and inflammatory profiles.

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Section: Discussionmentioning

confidence: 99%

“…One of the results observed was an increase in these receptors (RAGE) in the third group, most likely due to the higher amount of exogenous AGEs ingested [62]. …”

Section: Discussionmentioning

confidence: 99%

Choline and Cystine Deficient Diets in Animal Models with Hepatocellular Injury: Evaluation of Oxidative Stress and Expression of RAGE, TNF-α, and IL-1β

Santos

Araújo

Valentim

et al. 2015

Oxidative Medicine and Cellular Longevity

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“…High AGE levels, common in western diet, exacerbate liver injury, inflammation and fibrosis via oxidative stress, cytokine synthesis (TNF-a and IL-6), and through hepatic stellate cell activation. 85 Fructose over consumption, thereby contributes to development of obesity, dyslipidemia, and impaired glucose tolerance, producing AGEs responsible for producing dysfunctional proteins. 86 Therefore, AGE and its receptor pathway could be considered a new target for nutritional or pharmacological strategy to slow NAFLD progression.…”

Section: Fructosementioning

confidence: 99%

The Riddle of Nonalcoholic Fatty Liver Disease: Progression From Nonalcoholic Fatty Liver to Nonalcoholic Steatohepatitis

Sharma

Mitnala

Vishnubhotla

et al. 2015

Journal of Clinical and Experimental Hepatology

127

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Nonalcoholic fatty liver (NAFL) is an emerging global epidemic which progresses to nonalcoholic steatohepatitis (NASH) and cirrhosis in a subset of subjects. Various reviews have focused on the etiology, epidemiology, pathogenesis and treatment of NAFLD. This review highlights specifically the triggers implicated in disease progression from NAFL to NASH. The integrating role of genes, dietary factors, innate immunity, cytokines and gut microbiome have been discussed. ( J CLIN EXP HEPATOL 2015;5:147-158)

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“…HSCs also respond to IL-10, IL-6, and oncostatin M [138][139][140]. IL-6 is also produced by HSCs, and has been implicated in the regenerative response and, on the other hand, in the profibrogenic actions of glycotoxins [141,142]. IL-10 inhibits procollagen α(1) expression at the transcriptional level, and may have important anti-fibrogenic properties [139,143], as also indicated by the anti-fibrogenic actions of transgenic IL-10 expression in hepatocytes [144].…”

Section: Interleukins and Interferonsmentioning

confidence: 99%