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Fibroblast growth factor 21 promotes bone loss by potentiating the effects of peroxisome proliferator-activated receptor γ

Wei Wei; Paul A. Dutchak; Xunde Wang; Xunshan Ding; Xueqian Wang; Angie L. Bookout; Regina Goetz; Moosa Mohammadi; Robert D. Gerard; Paul C. Dechow; et al.

(Profiled Authors: Robert D Gerard; Steven A Kliewer; David J Mangelsdorf; Yihong Wan)

Proceedings of the National Academy of Sciences of the United States of America. 2012;109(8):3143-3148.


The endocrine hormone fibroblast growth factor 21 (FGF21) is a powerful modulator of glucose and lipid metabolism and a promising drug for type 2 diabetes. Here we identify FGF21 as a potent regulator of skeletal homeostasis. Both genetic and pharmacologic FGF21 gain of function lead to a striking decrease in bone mass. In contrast, FGF21 loss of function leads to a reciprocal high-bone-mass phenotype. Mechanistically, FGF21 inhibits osteoblastogenesis and stimulates adipogenesis from bonemarrowmesenchymal stem cells by potentiating the activity of peroxisome proliferator-activated receptor γ (PPAR-γ). Consequently, FGF21 deletion prevents the deleterious bone loss side effect of the PPAR-γ agonist rosiglitazone. Therefore, FGF21 is a critical rheostat for bone turnover and a key integrator of bone and energy metabolism. These results reveal that skeletal fragility may be an undesirable consequence of chronic FGF21 administration.

PMID: 22315431     PMCID: PMC3286969    

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