Journal
NATURE MEDICINE
Volume 19, Issue 9, Pages 1153-1156Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.3250
Keywords
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Funding
- Howard Hughes Medical Institute
- US National Institutes of Health [RL1GM084436, R01DK067158, R56DK089600, U19DK62434, GM007062]
- Robert A. Welch Foundation [I-1275, I-1558]
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)/National Institutes of Health (Specialized Cooperative Centers Program in Reproduction and Infertility Research (SCCPIR)) [U54-HD28934]
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Preventing reproduction during nutritional deprivation is an adaptive process that is conserved and essential for the survival of species. In mammals, the mechanisms that inhibit fertility during starvation are complex and incompletely understood(1-7). Here we show that exposure of female mice to fibroblast growth factor 21 (FGF21), a fasting-induced hepatokine, mimics infertility secondary to starvation. Mechanistically, FGF21 acts on the suprachiasmatic nucleus (SCN) in the hypothalamus to suppress the vasopressin-kisspeptin signaling cascade, thereby inhibiting the proestrus surge in luteinizing hormone. Mice lacking the FGF21 co-receptor, beta-Klotho, in the SCN are refractory to the inhibitory effect of FGF21 on female fertility. Thus, FGF21 defines an important liver-neuroendocrine axis that modulates female reproduction in response to nutritional challenge.
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