Paola Vitaglione1,2, G. Mazzone3, Vincenzo Lembo3, Giuseppe D’Argenio3, Andrea Salvo Rossi3, Maria Guido4, Marcella Savoia5, Federico Salomone6, Ilario Mennella1, Francesca De Filippis1,2, Danilo Ercolini1,2, N. Caporaso3,2, Filomena Morisco3,2
1Department of Agricultural Sciences, University of Naples Federico II, Portici, Italy
2Task Force on Microbiome Studies, University of Naples “Federico II”, Naples, Italy
3Department of Clinical Medicine and Surgery, Gastroenterology Unit, University of Naples Federico II, Naples, Italy
4Department of Medicine, University of Padua, Padua, Italy
5Department of Biochemistry and Medical Biotechnology, University of Naples Federico II, Naples, Italy
6Division of Gastroenterology, Azienda Sanitaria Provinciale di Catania, Catania, Italy
Tóm tắt
AbstractCoffee consumption is inversely associated with the risk of non-alcoholic fatty liver disease (NAFLD). A gap in the literature still exists concerning the intestinal mechanisms that are involved in the protective effect of coffee consumption towards NAFLD. In this study, twenty-four C57BL/6J mice were divided into three groups each receiving a standard diet, a high-fat diet (HFD) or an HFD plus decaffeinated coffee (HFD+COFFEE) for 12 weeks. Coffee supplementation reduced HFD-induced liver macrovesicular steatosis (P < 0·01) and serum cholesterol (P < 0·001), alanine aminotransferase and glucose (P < 0·05). Accordingly, liverPPAR- α(P < 0·05) and acyl-CoA oxidase-1 (P < 0·05) as well as duodenal ATP-binding cassette (ABC) subfamily A1 (ABCA1) and subfamily G1 (ABCG1) (P < 0·05) mRNA expressions increased with coffee consumption. Compared with HFD animals, HFD+COFFEE mice had more undigested lipids in the caecal content and higher free fatty acid receptor-1 mRNA expression in the duodenum and colon. Furthermore, they showed an up-regulation of duodenal and colonic zonulin-1 (P < 0·05), duodenal claudin (P < 0·05) and duodenal peptide YY (P < 0·05) mRNA as well as a higher abundance ofAlcaligenaceaein the faeces (P < 0·05). HFD+COFFEE mice had an energy intake comparable with HFD-fed mice but starting from the eighth intervention week they gained significantly less weight over time. Data altogether showed that coffee supplementation prevented HFD-induced NAFLD in mice by reducing hepatic fat deposition and metabolic derangement through modification of pathways underpinning liver fat oxidation, intestinal cholesterol efflux, energy metabolism and gut permeability. The hepatic and metabolic benefits induced by coffee were accompanied by changes in the gut microbiota.
