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• W4225418932 abstract "Bile acids classically known for their roles in dietary fat absorption are now recognized as hormones critical to regulating intestinal and metabolic function, including mucosal immune responses, epithelial proliferation/apoptosis, and transepithelial transport and barrier function. Downregulation of the nuclear bile acid receptor, farnesoid X receptor (FXR), in intestinal epithelium occurs in inflammatory bowel disease and colorectal cancer, whereas FXR activation prevents disease progression in pre-clinical models. Thus strategies to upregulate epithelial FXR expression have been proposed to treat such conditions. Previous studies suggest that some plant-derived phytochemicals have the capacity to modulate FXR activity. Plant sources have been reported to contain such phytochemicals, which are proposed to modulate FXR.The aim of the current study was to investigate the potential for developing plant extracts, rich in FXR-modulating phytochemicals, as a novel nutraceutical-based approach to treat and prevent intestinal diseases.T84 human colonic epithelial cells and primary cultures of murine colonic epithelial enteroids were employed to examine the effects of a common-dietary phytochemical, denoted here as KFS1, and a KFS1-rich plant extract on FXR expression and signaling in vitro. Ex vivo studies were carried out on human colonic tissue obtained during endoscopy with ethical approval from Beaumont Hospital. In vivo studies in C57BL/6 mice were carried out and proximal colonic tissue were examined with ethical approval from the HPRA. Expression of FXR and FGF19/15, an established marker of FXR activation, was assessed by qRT-PCR, ELISA and immunoblotting. Data are expressed as mean ± SEM for a series of n experiments.KFS1 treatment (5 µM; 24hrs) increased FXR mRNA and protein expression in T84 cells by 4.2 ± 0.4 (p<0.05; n = 4) and 1.7 ± 0.1 fold (p<0.05; n = 7) respectively. KFS1 also enhanced FGF19 protein expression in response to the FXR agonist GW4064 (5 µM), by 4.1 ± 0.5 fold (p<0.001; n = 7). Similarly KFS1 upregulated FXR expression by 2.1 ± 0.4 fold in human biopsies (p<0.05; n = 6). Oral KFS1 administration to mice had a tendency to upregulate colonic epithelial FXR signaling in vivo and increased FXR expression and GW4064-induced FGF15 by 2.3 ± 0.2 (p<0.01; n = 4) and 2.2 ± 0.1 fold (p<0.01; n = 4) in murine colonic enteroids. Finally a methanolic KFS1-rich plant extract, denoted QE1, verified by LC/MS to contain KFS1, increased FXR protein expression in vitro by 1.8 ± 0.2 fold (p<0.05; n = 5) and enhanced GW4064-induced FGF19 protein by 1.9 ± 0.1 fold (p<0.01; n = 9).Our data demonstrate that KFS1-containing plant extracts modulate expression and activity of FXR in the intestinal epithelium. Given the critical role of FXR in maintenance of gut health and metabolic function, such extracts have significant therapeutic and commercial potential to be developed as a novel first-in-class FXR-targeted nutraceutical for treatment and prevention of common intestinal disorders." @default.
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• W4225418932 date "2022-05-01" @default.
• W4225418932 modified "2023-09-27" @default.
• W4225418932 title "Nutraceutical targeting of the bile acid receptor, farnesoid X receptor, for intestinal disease" @default.
• W4225418932 doi "https://doi.org/10.1096/fasebj.2022.36.s1.r4543" @default.
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