Consumption of decaffeinated coffee protects against the development of early non-alcoholic steatohepatitis: Role of intestinal barrier function
| العنوان: | Consumption of decaffeinated coffee protects against the development of early non-alcoholic steatohepatitis: Role of intestinal barrier function |
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| المؤلفون: | Ina Bergheim, Finn Jung, Anika Nier, Cheng Jun Jin, Annette Brandt, Anja Baumann, José C. Fernández-Checa, Vicent Ribas, Carmen García-Ruiz |
| المساهمون: | Federal Ministry of Education and Research (Germany), Agencia Estatal de Investigación (España), Ministerio de Economía y Competitividad (España), Ministerio de Ciencia, Innovación y Universidades (España), Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas (España), Instituto de Salud Carlos III, Fundación BBVA, University of Vienna |
| المصدر: | Redox Biology Redox Biology, Vol 21, Iss, Pp-(2019) Digital.CSIC. Repositorio Institucional del CSIC instname |
| بيانات النشر: | Elsevier BV, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | 0301 basic medicine, Ir, insulin receptor, Tlr, toll-like receptor, Clinical Biochemistry, Ppia, peptidylprolyl isomerase A, DCE, decaffeinated coffee effect, DExDCE, interaction between diet and decaffeinated coffee, Biochemistry, Coffee, chemistry.chemical_compound, ZO-1, zonula occludens-1, Mice, 0302 clinical medicine, PCR, polymerase chain reaction, Coffees, Non-alcoholic Fatty Liver Disease, 3-NT, 3-nitrotyrosine, Intestinal Mucosa, DeCaf, decaffeinated coffee, lcsh:QH301-705.5, Barrier function, ANOVA, analysis of variance, lcsh:R5-920, NAS, NAFLD activity score, Atf, activating transcription factor 6, Fatty liver, Lbp, lipopolysaccharide binding protein, FFC, fat-, fructose- and cholesterol-rich diet, Endoplasmic Reticulum Stress, Immunohistochemistry, iNOS, medicine.anatomical_structure, Pdi, protein disulfide isomerase, Liver, GTT, glucose tolerance test, Female, medicine.symptom, lcsh:Medicine (General), Grp78, 78 kDa glucose-regulated protein, Research Paper, medicine.medical_specialty, NAFLD, non-alcoholic fatty liver disease, ALT, alanine transaminase, NASH, non-alcoholic steatohepatitis, Inflammation, Il, interleukin, Intestinal permeability, Nitric Oxide, Permeability, Nitric oxide, 03 medical and health sciences, Insulin resistance, Internal medicine, medicine, Animals, DE, diet effect, Irs, insulin receptor substrate, C, control, Edem1, ER degradation-enhancing alpha-mannosidase-like 1, iNOS, inducible NO-synthase, NO, nitric oxide, business.industry, Organic Chemistry, Chop, C/EBP homologous protein, Feeding Behavior, medicine.disease, Small intestine, Toll-Like Receptor 4, 030104 developmental biology, Endocrinology, Glucose, chemistry, lcsh:Biology (General), Dnajc3, DnaJ homolog subfamily C member 3, ER, endoplasmatic reticulum, Lipid Peroxidation, Steatohepatitis, business, Herpud1, homocysteine-responsive endoplasmatic reticulum-resident ubiquitin-like domain member 1 protein, 030217 neurology & neurosurgery, Biomarkers, Xbp1, X-box binding protein 1 |
| الوصف: | 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. Graphical abstract fx1 Highlights • decaffeinated coffee protects mice from the development of NAFLD. • decaffeinated coffee attenuated increased translocation of bacterial endotoxins. • decaffeinated coffee prevents diet-induced induction of iNOS in small intestine. |
| وصف الملف: | application/pdf |
| اللغة: | English |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b173ea7738b5f0fbb2100e259fb20393Test https://hdl.handle.net/11353/10.1172206Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....b173ea7738b5f0fbb2100e259fb20393 |
| قاعدة البيانات: | OpenAIRE |
| الوصف غير متاح. |