Fat diet and alcohol-induced steatohepatitis after LPS challenge in mice: Role of bioactive TNF and Th1 type cytokines

Olleros, Maria L.; Martín, María Luisa Moya; Vesin, Dominique; Fotio, Agathe Lambou; Santiago-Raber, Marie-Laure; Rubbia‐Brandt, Laura; Spahr, Laurent; Hadengue, Antoine; García, Irene

doi:10.1016/j.cyto.2008.07.001

Cited by 27 publications

(21 citation statements)

References 36 publications

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“…This was in agreement with Olleros et al [34] who reported that high fat in diet was associated with increased hepatic IL-6, interferon-gamma, and TNF-α. These cytokines play a major role in the inflammatory process that is the cornerstone in the development of steatohepatitis and its complications.…”

Section: Discussionsupporting

confidence: 92%

Ameliorative potential of omega 3 fatty acids and HMG-CoA reductase inhibitors on experimentally-induced non-alcoholic steatohepatitis

Kabel

Elmaaboud

Albarraq

2015

Prostaglandins, Leukotrienes and Essential Fatty Acids

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Section: Discussionsupporting

confidence: 92%

Ameliorative potential of omega 3 fatty acids and HMG-CoA reductase inhibitors on experimentally-induced non-alcoholic steatohepatitis

Kabel

Elmaaboud

Albarraq

2015

Prostaglandins, Leukotrienes and Essential Fatty Acids

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“…5, might result from the decrease in TNF-a production. Furthermore, activated production of TNF-a observed in steatohepatitis induced by fat/alcohol feeding with LPS injection was associated with increased expression of IFN-g (43).…”

Section: Discussionmentioning

confidence: 97%

IL-17 Is Necessary for Host Protection against Acute-Phase Trypanosoma cruzi Infection

Miyazaki

Hamano

Wang

et al. 2010

The Journal of Immunology

136

131

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“…The role of cytokine release from visceral white adipose tissue deserves special interest in the context of liver injury and hepatic insulin resistance since portal blood flow supplies the liver exclusively with the mediators secreted from visceral fat depots. The observation that LPS contributes to the induction of TNF in obesity came from mice which produced higher levels of inflammatory cytokines after feeding a high fat diet [76]. Augmented lymphocyte recruitment to the liver resulting in an increased inflammatory response to LPS was also observed [77].…”

Section: Tnf and Nf-jbmentioning

confidence: 95%

Diabetes and apoptosis: liver

Schattenberg

Schuchmann

2009

Apoptosis

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The liver is a central regulator of glucose homeostasis and stores or releases glucose according to metabolic demands. In insulin resistant states or diabetes the dysregulation of hepatic glucose release contributes significantly to the pathophysiology of these conditions. Acute or chronic liver disease can aggravate insulin resistance and the physiological effects of insulin on hepatocytes are disturbed. Insulin resistance has also been recognized as an independent risk factor for the development of liver injury. In the healthy liver tissue homeostasis is achieved through cell turnover by apoptosis and dysregulation of the physiological process resulting in too much or too little cell death can have potentially devastating effects on liver tissue. The delineation of the signaling pathways that mediate apoptosis changed the paradigms of understanding of many liver diseases. These signaling events include cell surface based receptor-ligand systems and intracellular signaling pathways that are regulated through kinases on multiple levels. The dissection of these signaling pathways has shown that the regulators of apoptosis signaling events in hepatocytes can also modulate insulin signaling pathways and that mediators of insulin resistance in turn influence liver cell apoptosis. This review will summarize the potential crosstalk between apoptosis and insulin resistance signaling events and discuss the involved mediators.

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Fat diet and alcohol-induced steatohepatitis after LPS challenge in mice: Role of bioactive TNF and Th1 type cytokines

Cited by 27 publications

References 36 publications

Ameliorative potential of omega 3 fatty acids and HMG-CoA reductase inhibitors on experimentally-induced non-alcoholic steatohepatitis

Ameliorative potential of omega 3 fatty acids and HMG-CoA reductase inhibitors on experimentally-induced non-alcoholic steatohepatitis

IL-17 Is Necessary for Host Protection against Acute-Phase Trypanosoma cruzi Infection

Diabetes and apoptosis: liver

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