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Direct in vivo evidence demonstrates that Fgf15 is critical in stimulating the phases of priming and termination of liver regeneration that are critical for cell survival and liver-size determination, independent of bile acids levels.
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Study shows that FXR is phosphorylated at Y67 by non-receptor tyrosine kinase, Src, in response to postprandial Fgf15 which is critical for its nuclear localization and transcriptional regulation of bile acids (BA) levels. Liver-specific expression of phospho-defective Y67F-FXR in mice results in impaired responses to acute BA feeding and exacerbates cholestatic pathologies upon drug-induced hepatobiliary insults.
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Taken together, these results suggested that FGF19, through the anti-oxidative defense system, attenuated the development of diabetic cardiomyopathy and restored cardiac function.
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ileal FGF15/19 to hepatic FGFR4 axis is activated and promotes liver regeneration (LR) after partial hepatectomy (PH) in mice, supporting the potential of ileal FGF15/19 to hepatic FGFR4 axis-targeted therapy to enhance LR after PH
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FRS2alpha-mediated pathways are essential for the FGF15/FGF19-FGFR4 signaling axis to control bile acid homeostasis.
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Together, our results show that SuFu promotes cerebellar radial precursor differentiation to neurons. SuFu function is mediated in part by GLI3R and down-regulation of Fgf15 expression.
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Results show a reciprocal regulation of adiponectin and FGF19 gene expression in mice.
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Tumorigenicity was assessed in three mouse models (db/db, diet-induced obese, and multi-drug resistance 2 [Mdr2]-deficient) following continuous exposure to FGF19 or FGF15 via adeno-associated viral-mediated gene delivery.
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These data identify hypothalamic Fgf15 as a regulator of glucagon secretion.
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Intestinal sensing of highly elevated levels of conjugated bile acids in blood promotes FGF15 signaling, reducing hepatic bile acid synthesis and modulating bile acid transporters.
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Fgf15 is the sonic hedgehog downstream signal to control thalamic regionalization, neurogenesis, and neuronal differentiation by regulating the expression and mutual segregation of neurogenic and proneural regulatory genes.
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human microbiota was able to reduce the levels of tauro-beta-muricholic acid and induce expression of FXR target genes Fgf15 and Shp in ileum after long-term colonization. We show that a human microbiota can change BA composition and induce FXR signaling in colonized mice, but the levels of secondary BAs produced are lower than in mice colonized with a mouse microbiota
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FGF15 improves lipid homeostasis and reduces bile acid synthesis, but promotes fibrosis during the development of non-alcoholic steatohepatitis
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This study demonstrates that the FGF19-SHP-LSD1 axis maintains homeostasis by suppressing unnecessary autophagic breakdown of cellular components, including lipids, under nutrient-rich postprandial conditions.
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The elevation in circulating levels of adiponectin and Fgf15 led to normalized hepatic and serum levels of bile acids, limited hepatic accumulation of toxic bile, attenuated inflammation, and amelioration of liver injury in the ethanol-fed mNT knockout mice.
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This study reveals SHP as a global transcriptional partner of SREBP-2 in regulation of sterol biosynthetic gene networks and provides a potential mechanism for cholesterol-lowering action of FGF19.
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we suggest that considerable mechanistic differences exist between humans and mice with regard to the nuclear receptors controlling the VitA-FGF15/19 axis.
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Ileal Fgf15 expression is a potent inhibitor of bile acid synthesis.
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Protective effects of farnesoid X receptor on hepatic lipid accumulation are mediated by hepatic FXR and are independent of intestinal FGF15 signaling.
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In mice with humanized livers human hepatocytes do not recognize FGF-15 produced by mouse intestine, resulting in up-regulation of bile acid synthesis enlargement of the bile acid pool, affecting the hepatostat.
