Fatty liver disease: The liver labyrinth

Morgan, Branwen

doi:10.1038/516s8a

Cited by 11 publications

(8 citation statements)

References 4 publications

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“…Also, the Office for National Statistics in the UK indicated that liver disease is the fifth most common cause of death after heart disease, stroke, chest disease and cancer (14). Particularly, hepatocellular carcinoma caused by hepatitis B surface antigen is among the first three causes of death from cancer in men, and a major cause of cancer in women (15)(16)(17). Substantial evidence has been collected confir ming the relationship between hepatitis and hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Resolvin D1 and E1 alleviate the progress of hepatitis toward liver cancer in long-term concanavalin A-induced mice through inhibition of NF-κB activity

et al. 2015

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Resolvins, an endogenous lipid mediator derived from eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) of fish oil, has been reported to have anti-inflammatory and antitumor effect in various pathogenic processes. However, there are no studies about the effects of resolvin D1 and E1 on concanavalin A-induced hepatitis. Hence, the present study is to illustrate whether resolvin D1 and E1 inhibit concanavalin A-induced liver injury, liver cancer and underlying mechanisms by which they may recover. C57BL/6 mice were pretreated with resolvin D1 and E1 for 4 h, and then injected with concanavalin A for 12 h. Subsequently, blood and liver tissue were collected at 0, 2, 4, 8 and 12 h for different analysis. Analysis of inflammatory cytokines indicated that the inhibition of necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-2, IL-1β and IL-6 could be performed by resolvin D1 and E1. Moreover, Toll-like receptor (TLR) 4 expression, NF-κB and AP-1 activity also have been confirmed to have key roles in the development of liver injury. They were significantly suppressed in the treatment group, compared to model. In addition, resolvin D1 and E1 markedly downregulated CD4+ and CD8+ cell infiltration in the liver. A long-term concanavalin A treatment for 32 weeks was performed to analyze the changes of hepatitis to liver cancer and the antitumor effect of resolving D1 and E1. These results indicated that resolvin D1 and E1 prevent concanavalin A-induced liver injury and the changes of hepatitis to liver cancer in mice through inhibition of inflammatory cytokine secretion and NF-κB/AP-1 activity. Thus, they could be novel target to be considered in the process of finding sufficient drug to protect against various forms of hepatitis and liver cancer.

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Section: Discussionmentioning

confidence: 99%

Resolvin D1 and E1 alleviate the progress of hepatitis toward liver cancer in long-term concanavalin A-induced mice through inhibition of NF-κB activity

et al. 2015

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“…The strong medical interest in a better understanding of the molecular processes underlying the regulation of liver metabolism arises from the fact that an ongoing metabolic imbalance of the organ, e.g., due to excessive intake of drugs, alcohol or fructose, may result in an abnormal accumulation of lipids (steatosis) thereby increasing the risk of developing serious liver diseases such as hepatitis, cirrhosis, and cancer 3 . Aiming at the in vivo assessment of liver metabolism, we developed a kinetic multi-pathway model of hepatocytes with hitherto unprecedented scope and level of detail.…”

Section: Introductionmentioning

confidence: 99%

HEPATOKIN1 is a biochemistry-based model of liver metabolism for applications in medicine and pharmacology

et al. 2018

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The epidemic increase of non-alcoholic fatty liver diseases (NAFLD) requires a deeper understanding of the regulatory circuits controlling the response of liver metabolism to nutritional challenges, medical drugs, and genetic enzyme variants. As in vivo studies of human liver metabolism are encumbered with serious ethical and technical issues, we developed a comprehensive biochemistry-based kinetic model of the central liver metabolism including the regulation of enzyme activities by their reactants, allosteric effectors, and hormone-dependent phosphorylation. The utility of the model for basic research and applications in medicine and pharmacology is illustrated by simulating diurnal variations of the metabolic state of the liver at various perturbations caused by nutritional challenges (alcohol), drugs (valproate), and inherited enzyme disorders (galactosemia). Using proteomics data to scale maximal enzyme activities, the model is used to highlight differences in the metabolic functions of normal hepatocytes and malignant liver cells (adenoma and hepatocellular carcinoma).

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“…In addition to the risk of heart disease, 22 diabetes, 23 and cancer, 24 overweight and obesity also increase the risk of nonalcoholic fatty liver disease (NAFLD), which is a spectrum of liver abnormalities such as simple steatosis (steatosis without hepatocellular injury), nonalcoholic steatohepatitis (steatosis with inflammation and hepatocyte ballooning degeneration), fibrosis, cirrhosis and, ultimately, hepatocellular carcinoma. 25,26 Previous studies have shown that the liver is a major organ for deposition of nanoparticles after absorption. 27−31 A single oral dose of Ag NPs induced acute inflammation of the liver in healthy male BALB/c mice, as evidenced by lymphocyte infiltration and increased expression of genes related to inflammation.…”

Section: ■ Introductionmentioning

confidence: 99%

Oral Exposure to Silver Nanoparticles or Silver Ions May Aggravate Fatty Liver Disease in Overweight Mice

Jia

Zhou

et al. 2017

Environ. Sci. Technol.

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As the applications and environmental release of silver ions and nanoparticles are increasing, increasing human exposure to these pollutants has become an emerging health concern. The impeding effects of such pollutants on susceptible populations are severely under-studied. Here, we demonstrate that silver nanoparticles (Ag NPs), at a dose that causes no general toxicity in normal mice, promotes the progression of fatty liver disease from steatosis to steatohepatitis only in overweight mice. Exposure to Ag ions induces the same effects in overweight mice. Ag NPs rather than Ag ions cause this disease progression based on our findings that Ag ions are partly reduced to Ag NPs in fatty livers, and the toxic effect is correlated with the liver dose of Ag NPs, not Ag ions. Furthermore, the Ag NP-induced pro-inflammatory activation of Kupffer cells in the liver, enhancement of hepatic inflammation, and suppression of fatty acid oxidation are identified as key factors in the underlying mechanisms.

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Fatty liver disease: The liver labyrinth

Cited by 11 publications

References 4 publications

Resolvin D1 and E1 alleviate the progress of hepatitis toward liver cancer in long-term concanavalin A-induced mice through inhibition of NF-κB activity

Resolvin D1 and E1 alleviate the progress of hepatitis toward liver cancer in long-term concanavalin A-induced mice through inhibition of NF-κB activity

HEPATOKIN1 is a biochemistry-based model of liver metabolism for applications in medicine and pharmacology

Oral Exposure to Silver Nanoparticles or Silver Ions May Aggravate Fatty Liver Disease in Overweight Mice

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