Author information
1
Department of Nutritional Sciences, R.F. Molecular Nutritional Science, University of Vienna, Vienna, Austria.
2
Institute of Nutrition, SD Model Systems of Molecular Nutrition, Friedrich-Schiller University Jena, Jena, Germany.
3
Cell Death and Proliferation, Institute of Biomedical Research of Barcelona, Spanish National Research Council, Barcelona, Spain; Liver Unit, Clinical and Provincial Hospital of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer and CIBEREHD, Barcelona, Spain.
4
Cell Death and Proliferation, Institute of Biomedical Research of Barcelona, Spanish National Research Council, Barcelona, Spain; Liver Unit, Clinical and Provincial Hospital of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer and CIBEREHD, Barcelona, Spain; Research Center for ALPD, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
5
Department of Nutritional Sciences, R.F. Molecular Nutritional Science, University of Vienna, Vienna, Austria. Electronic address: ina.bergheim@univie.ac.at.
Abstract
BACKGROUND:
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide lacking universally accepted therapies. Studies suggest that coffee consumption is associated with a reduced risk of NAFLD; however, molecular mechanisms and ingredients involved remain to be fully understood. Here, we determined the effects of regular intake of decaffeinated coffee on the development of NAFLD in mice, and molecular mechanisms involved.
METHODS:
Female C57BL/6J mice (n = 6-7/ group) were pair-fed either a liquid control diet (C) or fat-, fructose- and cholesterol-rich diet (FFC) +/- decaffeinated coffee (DeCaf, 6 g/kg BW) for 4 days or 6 weeks. Indices of liver damage, hepatic inflammation and parameters of insulin resistance and intestinal permeability as well as nitric oxide system were determined.
RESULTS:
Early signs of insulin resistance and non-alcoholic steatohepatitis (NASH) found after 6 weeks of FFC feeding were significantly lower in FFC+DeCaf-fed mice when compared to FFC-fed animals. Moreover, elevation of portal endotoxin levels and loss of tight junction proteins in proximal small intestine found in FFC-fed mice were significantly attenuated in FFC+DeCaf-fed animals. These beneficial effects of DeCaf were associated with a protection against the significant induction of inducible NO-synthase protein levels and 3-nitrotyrosine protein adducts found in proximal small intestine of FFC-fed mice. Similar protective effects of DeCaf were also found in mice fed the FFC diet short-term.
CONCLUSION:
Our results suggest that protective effects of DeCaf on the development of NAFLD are at least in part related to maintaining intestinal barrier function.