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[PubMed] [Google Scholar] 30.Crespo A, Filla MB, Russell SW, Murphy WJ

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J Ethnopharmacol 147:547563

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FGF19 is also an attractive therapeutic target in NASH (table 1) where NGM282/aldafermin, significantly reduced hepatic fat content, serum aminotransferase levels and non-invasive fibrosis markers while histological improvement of fibrosis or resolution of NASH did not reach statistical significance after 24 weeks of treatment.136 Interestingly, enrichment of Veillonella, a BA-sensitive bacteria whose enrichment is enabled by NGM282/aldafermin, may be a marker for therapeutic response.137 Side effects of NGM282 are mostly of gastrointestinal origin but also include increases in LDL-cholesterol,138 which can be managed by statins.139 These findings emphasise that FXR/FGF-19-mediated suppression of BA synthesis will result in increased hepatocellular cholesterol levels with subsequent downregulation of LDL-receptor and increased serum cholesterol levels.88 This is an important consideration for any FXR-pathway targeted therapy in NASH and associated cardiovascular risk.7 Peroxisome proliferator-activated receptors PPARs are a group of NRs that fine tune lipid and glucose metabolism and regulate inflammation and fibrosis.140 141 The three isoforms, PPAR, PPAR and PPAR (also known as ), are expressed in different parenchymal and non-parenchmal liver cell compartments, making them highly attractive targets for therapy of metabolic142 and cholestatic liver diseases.143 Various drugs target PPAR (fibrates), PPAR (thiazolidinediones/glitazones), PPAR (seladelpar) or simultaneously two PPAR isoforms (PPAR/glitazars and PPAR/elafibranor)