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Lookup NU author(s): Professor Brian WalkerORCiD, Professor Andreas Schedl
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Fuelled by the obesity epidemic, there is considerable interest in the developmental origins of white adipose tissue (WAT) and the stem and progenitor cells from which it arises. Whereas increased visceral fat mass is associated with metabolic dysfunction, increased subcutaneous WAT is protective. There are six visceral fat depots: perirenal, gonadal, epicardial, retroperitoneal, omental and mesenteric, and it is a subject of much debate whether these have a common developmental origin and whether this differs from that for subcutaneous WAT. Here we show that all six visceral WAT depots receive a significant contribution from cells expressing Wt1 late in gestation. Conversely, no subcutaneous WAT or brown adipose tissue arises from Wt1-expressing cells. Postnatally, a subset of visceral WAT continues to arise from Wt1-expressing cells, consistent with the finding that Wt1 marks a proportion of cell populations enriched in WAT progenitors. We show that all visceral fat depots have a mesothelial layer like the visceral organs with which they are associated, and provide several lines of evidence that Wt1-expressing mesothelium can produce adipocytes. These results reveal a major ontogenetic difference between visceral and subcutaneous WAT, and pinpoint the lateral plate mesoderm as a major source of visceral WAT. They also support the notion that visceral WAT progenitors are heterogeneous, and suggest that mesothelium is a source of adipocytes. © 2014 Macmillan Publishers Limited.
Author(s): Chau Y-Y, Bandiera R, Serrels A, Martinez-Estrada OM, Qing W, Lee M, Slight J, Thornburn A, Berry R, Mchaffie S, Stimson RH, Walker BR, Chapuli RM, Schedl A, Hastie N
Publication type: Article
Publication status: Published
Journal: Nature Cell Biology
Year: 2014
Volume: 16
Issue: 4
Pages: 367-375
Print publication date: 01/04/2014
Online publication date: 09/03/2014
Acceptance date: 27/01/2014
ISSN (print): 1465-7392
ISSN (electronic): 1476-4679
Publisher: Nature Publishing Group
URL: https://doi.org/10.1038/ncb2922
DOI: 10.1038/ncb2922
PubMed id: 24609269
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