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  • Wiley  (2)
  • Enrich, Barbara  (2)
  • 1
    In: Liver International, Wiley, Vol. 38, No. 6 ( 2018-06), p. 1095-1101
    Abstract: Chronic alcohol consumption and alcoholic liver disease ( ALD ) afflicts individuals with substantial morbidity and mortality with limited treatment options available. Hepatic inflammation, triggered by activated Kupffer cells, is a driving force in alcoholic liver disease. Interleukin 37 ( IL ‐37) exerts anti‐inflammatory effects in hepatic diseases, however, the impact of Interleukin 37 on alcoholic liver disease is unknown. In this study, we addressed the role of Interleukin 37 in alcoholic liver disease. Methods We utilized Interleukin 37 expressing transgenic mice and human recombinant Interleukin 37 in models of alcoholic liver disease. Interleukin 37 expression was measured in liver samples of 20 alcoholic steatohepatitis and 36 non‐alcoholic fatty liver disease patients. Results Interleukin 37 transgenic mice are not protected against hepatic injury and inflammation in alcoholic liver disease. Ethanol suppressed Interleukin 37 expression in transgenic mice. Alcoholic steatohepatitis ( ASH ) patients similarly exhibited reduced Interleukin 37 expression when compared to non‐alcoholic fatty liver disease ( NAFLD ) patients. Human recombinant Interleukin 37 ameliorated hepatic inflammation in a binge drinking model of alcoholic liver disease. Conclusion We provide evidence for an exogenous noxae that suppresses Interleukin 37 expression which limits its anti‐inflammatory effects in alcoholic liver disease.
    Type of Medium: Online Resource
    ISSN: 1478-3223 , 1478-3231
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2124684-1
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  • 2
    In: Liver International, Wiley, Vol. 37, No. 2 ( 2017-02), p. 299-306
    Abstract: Obesity and its related co‐morbidities such as non‐alcoholic fatty liver disease ( NAFLD ) are increasing dramatically worldwide. The genetic variation in Patatin‐like phospholipase domain‐containing protein 3 ( PNPLA 3 ), which is also called adiponutrin ( ADPN ), in residue 148 (I148M, rs738409) has been associated with NAFLD . However, the regulation and function of PNPLA 3 in metabolic diseases remains unclear. Laparoscopic gastric banding ( LAGB ) of severely obese patients reduces body weight, liver and adipose tissue inflammation. In this study, we investigated whether weight loss induced by LAGB affected PNPLA 3 expression in hepatic and adipose tissue. Methods Liver and subcutaneous adipose tissue samples were collected from 28 severely obese patients before and 6 months after LAGB . PNPLA 3 expression was assessed by quantitative real‐time PCR . To understand whether inflammatory stimuli regulated PNPLA 3 expression, we studied the effect of tumour necrosis factor alpha ( TNF α) and lipopolysaccharide ( LPS ) on PNPLA 3 expression in human adipocytes and hepatocytes. Results PNPLA 3 was strongly expressed in the liver and clearly detectable in subcutaneous adipose tissue of obese patients. Weight loss induced by LAGB of severely obese patients led to significantly increased adipose, but not hepatic, tissue expression of PNPLA 3 . Subcutaneous PNPLA 3 expression negatively correlated with body‐mass‐index, fasting glucose and fasting insulin. TNF α potently suppressed PNPLA 3 expression in adipocytes but not hepatocytes. Conclusions Weight loss induced by LAGB restored adipose tissue PNPLA 3 expression which is suppressed by TNF α. Further studies will be required to determine the functional impact of PNPLA 3 and its related genetic variation on adipose tissue inflammation and NAFLD .
    Type of Medium: Online Resource
    ISSN: 1478-3223 , 1478-3231
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2124684-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
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