Activin Signaling Mediates Muscle-to-Adipose Communication in a Mitochondria Dysfunction-Associated Obesity Model
Activin signaling mediates muscle-to-adipose communication in a mitochondria dysfunction-associated obesity model.pdf (1.302Mb)
Access StatusFull text of the requested work is not available in DASH at this time ("restricted access"). For more information on restricted deposits, see our FAQ.
MetadataShow full item record
CitationSong, Wei, Edward Owusu-Ansah, Yanhui Hu, Daojun Cheng, Xiaochun Ni, Jonathan Zirin, Norbert Perrimon. "Activin Signaling Mediates Muscle-to-Adipose Communication in a Mitochondria Dysfunction-Associated Obesity Model." Proceedings of the National Academy of Sciences 114, no. 32 (2017): 8596-8601. DOI: 10.1073/pnas.1708037114
AbstractMitochondrial perturbation-associated dysregulation of one organ has been shown to nonautonomously affect the functions of other organs in both vertebrates and invertebrates. Using Drosophila as a genetic model organism, we characterized mitochondrial synchrony dysregulation across organs and uncovered that mitochondrial perturbation caused by complex I disruption in muscles remotely impairs mitochondrial function and lipid mobilization in the fat body, leading to obesity. We further identified that the TGF-β ligand Actβ, which is autonomously increased by muscular mitochondrial perturbation, mediates muscle-to-fat-body communication and synchronized mitochondrial dysregulation.
Citable link to this pagehttps://nrs.harvard.edu/URN-3:HUL.INSTREPOS:37368034
- HMS Scholarly Articles