Fibroblast growth factor 19-targeted therapies for the treatment of metabolic disease. (May 2015)

• Record Type: Journal Article
• Authors: Rysz, Jacek; Gluba-Brzózka, Anna; Mikhailidis, Dimitri P; Banach, Maciej
• Is Part Of: Expert opinion on investigational drugs. Volume 24:Number 5(2015:May)
• Page Start: 603
• Page End: 610
• Publication Date: 2015-05
• Subjects: Drugs -- Design -- Periodicals; Drugs, Investigational -- Bibliography; Drugs, Investigational -- Periodicals; 615.1
• DOI: 10.1517/13543784.2015.1006357
• Languages: English
• ISSNs: 1354-3784

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p> <bold> <italic>Introduction:</italic> </bold> Fibroblast growth factors (FGFs) belong to the FGF superfamily with diverse biological functions, including proliferation, cellular differentiation, wound repair, angiogenesis and tumorigenesis. The ability to reduce liver fat content and concentrations of triglycerides, total cholesterol and plasma glucose, and to improve sensitivity and limit pro-lipogenic properties of insulin, makes FGF19 a promising therapeutic target for the treatment of metabolic syndrome. FGF19 regulates bile acid biosynthesis in the bile duct, glucose metabolism and vitamin D and phosphate homeostasis, raises the metabolic rate, reduces body weight, and ameliorates diabetes in mice. The therapeutic potential of FGF19 to treat metabolic disorders has been widely studied in animal models, but currently there are no reports concerning its use in humans.</p> <p> <bold> <italic>Areas covered:</italic> </bold> The following article highlights the metabolic effects and mechanism of action of FGF19. It also discusses the potential therapies that target FGF19.</p> <p> <bold> <italic>Expert opinion:</italic> </bold> FGF19 is emerging as a new target for the therapy of metabolic disorders, including diabetes. The results obtained from animal models are promising. However, there is still much to be done before the translation of these effects into practice will be possible.</p> </abstract>