@article{02cb31c9cd4a48ddbb444b57d332dbe8,
title = "FGF21 acts centrally to induce sympathetic nerve activity, energy expenditure, and weight loss",
abstract = "The mechanism by which pharmacologic administration of the hormone FGF21 increases energy expenditure to cause weight loss in obese animals is unknown. Here we report that FGF21 acts centrally to exert its effects on energy expenditure and body weight in obese mice. Using tissue-specific knockout mice, we show that βKlotho, the obligate coreceptor for FGF21, is required in the nervous system for these effects. FGF21 stimulates sympathetic nerve activity to brown adipose tissue through a mechanism that depends on the neuropeptide corticotropin-releasing factor. Our findings provide an unexpected mechanistic explanation for the strong pharmacologic effects of FGF21 on energy expenditure and weight loss in obese animals.",
author = "Owen, {Bryn M.} and Xunshan Ding and Morgan, {Donald A.} and Coate, {Katie Colbert} and Bookout, {Angie L.} and Kamal Rahmouni and Kliewer, {Steven A.} and Mangelsdorf, {David J.}",
note = "Funding Information: We thank Yuan Zhang, Heather Lawrence, Kevin Vale, and Sofya Perelman for technical assistance and Birgitte Andersen (Novo Nordisk) for providing human recombinant FGF21. This work was supported by National Institutes of Health grants R01DK067158 (S.A.K. and D.J.M.), 1F32DK098908 (K.C.C), GM007062 (A.L.B.), and HL084207 (K.R.); the Robert A. Welch Foundation (grant I-1558 to S.A.K. and grant I-1275 to D.J.M.); the American Heart Association (14EIA18860041 to K.R.); and the Howard Hughes Medical Institute (to K.C.C. and D.J.M.). X.D. is an employee and stockholder of NGM Biopharmaceuticals. The recombinant FGF21 was provided by Novo Nordisk. Publisher Copyright: {\textcopyright} 2014 Elsevier Inc.",
year = "2014",
month = oct,
day = "7",
doi = "10.1016/j.cmet.2014.07.012",
language = "English (US)",
volume = "20",
pages = "670--677",
journal = "Cell Metabolism",
issn = "1550-4131",
publisher = "Cell Press",
number = "4",
}