| Literature DB >> 28538730 |
Peng Liu1, Yaoting Ji1,2, Tony Yuen1, Elizabeth Rendina-Ruedy3, Victoria E DeMambro3, Samarth Dhawan1, Wahid Abu-Amer1, Sudeh Izadmehr1, Bin Zhou4, Andrew C Shin1, Rauf Latif1, Priyanthan Thangeswaran1, Animesh Gupta1, Jianhua Li1, Valeria Shnayder1, Samuel T Robinson4, Yue Eric Yu4, Xingjian Zhang4, Feiran Yang4, Ping Lu1, Yu Zhou1, Ling-Ling Zhu1, Douglas J Oberlin1, Terry F Davies1, Michaela R Reagan3, Aaron Brown3, T Rajendra Kumar5, Solomon Epstein1, Jameel Iqbal6, Narayan G Avadhani7, Maria I New1, Henrik Molina8, Jan B van Klinken9, Edward X Guo4, Christoph Buettner1, Shozeb Haider10, Zhuan Bian2, Li Sun1, Clifford J Rosen3, Mone Zaidi1.
Abstract
Menopause is associated with bone loss and enhanced visceral adiposity. A polyclonal antibody that targets the β-subunit of the pituitary hormone follicle-stimulating hormone (Fsh) increases bone mass in mice. Here, we report that this antibody sharply reduces adipose tissue in wild-type mice, phenocopying genetic haploinsufficiency for the Fsh receptor gene Fshr. The antibody also causes profound beiging, increases cellular mitochondrial density, activates brown adipose tissue and enhances thermogenesis. These actions result from the specific binding of the antibody to the β-subunit of Fsh to block its action. Our studies uncover opportunities for simultaneously treating obesity and osteoporosis.Entities:
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Year: 2017 PMID： 28538730 PMCID： PMC5651981 DOI： 10.1038/nature22342
Source DB: PubMed Journal: Nature ISSN： 0028-0836 Impact factor: 49.962