Progression of non-alcoholic steatosis to steatohepatitis and fibrosis parallels cumulative accumulation of danger signals that promote inflammation and liver tumors in a high fat–cholesterol–sugar diet model in mice

Michal Ganz; Terence N. Bukong; Tímea Csák; Banishree Saha; Jin‐Kyu Park; Aditya Ambade; Karen Kodys; Gyöngyi Szabó

doi:10.1186/s12967-015-0552-7

June 15, 2015Journal of Translational MedicineOpen Access

Progression of non-alcoholic steatosis to steatohepatitis and fibrosis parallels cumulative accumulation of danger signals that promote inflammation and liver tumors in a high fat–cholesterol–sugar diet model in mice

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Key Points

To evaluate how long-term consumption of a high-fat, high-cholesterol, and high-sugar diet drives the progression of non-alcoholic fatty liver disease to steatohepatitis, fibrosis, and tumorigenesis in mice.
Maintained mice on a high-fat, high-cholesterol, and high-sugar diet (HF-HC-HSD) for 49 weeks.
Tracked liver pathophysiology, accumulation of sterile and microbial danger signals, inflammasome activation, and M1/M2 macrophage ratios across disease progression.
A 49-week HF-HC-HSD regimen induced the full spectrum of non-alcoholic fatty liver disease observed in humans, progressing through steatohepatitis, fibrosis, and liver tumors.
Disease progression directly paralleled the progressive accumulation of sterile and microbial danger signals, inflammasome activation, and altered M1/M2 cell ratios.

Implication

Demonstrates that high fat–cholesterol–sugar feeding drives progressive inflammation and liver tumors in mice, indicating danger signal accumulation fuels severe fatty liver disease.

Abstract

HF-HC-HSD over 49 weeks induces the full spectrum of liver pathophysiologic changes that characterizes the progression of NAFLD in humans. NAFLD progression to NASH, fibrosis and liver tumor follows progressive accumulation of sterile and microbial danger signals, inflammasome activation, altered M1/M2 cell ratios that likely contribute to NASH progression and hepatic tumor formation.

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Cite This Study

Ganz et al. (2015) studied this question.

synapsesocial.com/papers/69daba544e9a02dbaa684058 https://doi.org/10.1186/s12967-015-0552-7

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Progression of non-alcoholic steatosis to steatohepatitis and fibrosis parallels cumulative accumulation of danger signals that promote inflammation and liver tumors in a high fat–cholesterol–sugar diet model in mice

Key Points

Implication

Abstract

Discussion

Cite This Study

Progression of non-alcoholic steatosis to steatohepatitis and fibrosis parallels cumulative accumulation of danger signals that promote inflammation and liver tumors in a high fat–cholesterol–sugar diet model in mice

Key Points

Implication

Abstract

Discussion

Cite This Study

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