FGF21 : un lien entre reproduction et métabolisme

Loss-of-function mutations in FGFR1 are a frequent cause of congenital hypogonadotropic hypogonadism (CHH), a severe form of gonadotropin-releasing hormone (GnRH) deficiency, in males and females characterized by absent puberty and infertility. FGFR1 mutations also predispose females to hypothalamic...

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Bibliographic Details
Published inAnnales d'endocrinologie Vol. 75; no. 5; p. 250
Main Author Pitteloud, N
Format Journal Article
LanguageFrench
Published Elsevier Masson SAS 01.10.2014
Subjects
Endocrinology & Metabolism
Internal Medicine
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Summary:Loss-of-function mutations in FGFR1 are a frequent cause of congenital hypogonadotropic hypogonadism (CHH), a severe form of gonadotropin-releasing hormone (GnRH) deficiency, in males and females characterized by absent puberty and infertility. FGFR1 mutations also predispose females to hypothalamic amenorrhea (HA), a milder and reversible form of GnRH deficiency associated with stress and/or energy deficits. FGF21 is an important metabolic regulator, which signals through a complex of FGFR1c with its co-receptor ß-Klotho. Interestingly, female Fgf21 transgenic ( Tg ) mice are resistant to high fat diet and exhibit GnRH deficiency and infertility. We further demonstrated that loss-of-function KLB mutations underlie congenital GnRH deficiency while Klb–/– mice exhibit delayed puberty supporting a role for KLB in reproduction. These findings highlight FGF21 as an important link between metabolism and reproduction.
ISSN:0003-4266
DOI:10.1016/j.ando.2014.07.005