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Fibroblast growth factor 19 (FGF19) is increasingly recognized as a key hormone regulating many functions. A recent publication by Luo et al. In Science Translational Medicine has advanced understanding of the diverse actions of FGF19 and has suggested how therapeutics with this protein may be optimized ().
FGF19 in humans is a 24 kDa protein which is syntenic with FGF15 in rodents; both have similar tissue distribution and actions and are sometimes known as FGF15/19 (). FGF15/19, together with FGF21 and FGF23, are members of the larger group of fibroblast growth factors and share the property of low heparin sulfate binding, which allows them to function as circulating endocrine molecules with effects on distant tissues. FGF15/19 has major effects regulating hepatic bile acid synthesis () and also acts on carbohydrate and lipid metabolism (). FGF21 also has metabolic functions, and FGF23 is the key hormone regulating phosphate homeostasis. These effects are produced through FGF receptors (FGFR).
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FGF15/19 at physiological levels acts preferentially through FGFR4, which forms complexes with β-Klotho, and produces intracellular effects through kinase actions (,). FGF19 is synthesized in the ileum in response to bile acid absorption. Bile acids bind to farnesoid X receptor (FXR) and potently activate transcription of FGF15 in mouse intestine () and FGF19 in human ileal explants [reviewed in ()]. FGF19 enters the portal venous circulation and inhibits new bile acid synthesis in the liver by decreasing CYP7A1 activity, thus providing negative feedback. Serum FGF19 increases after meals () and is much lower in patients who have had ileal resection or with inflammation in Crohn’s disease (-). Impaired regulation of bile acid synthesis by FGF19 has been proposed to be a causative factor in the common disorder known as primary bile acid diarrhea or idiopathic bile acid malabsorption ().
Furthermore, obeticholic acid, a semi-synthetic modified bile acid and a potent FXR agonist, stimulated FGF19 production and improved symptoms in these patients (). A role for defective FGF15/19 in bile acid-induced diarrhea is further supported by evidence from mouse models with knock-out of the components of FGF15 system ( Fgf15, Fgfr4 and Klb) which have increased fecal bile acid loss, increased synthesis and a larger bile acid pool size.Additionally, severe diarrhea resulted in monkeys when FGF19 was neutralized with antibodies [reviewed in ()]. Therapy to increase FGF19 actions seems to be a promising approach to treating this form of chronic diarrhea associated with excess bile acid production.