Author
Listed:
- ShengPeng Wang
(Max Planck Institute for Heart and Lung Research, Department of Pharmacology
Xi’an Jiaotong University Health Science Center, Key Laboratory of Environment and Genes Related to Diseases)
- Shuang Cao
(Max Planck Institute for Heart and Lung Research, Department of Pharmacology
Xi’an Jiaotong University Health Science Center, Key Laboratory of Environment and Genes Related to Diseases)
- Malika Arhatte
(Université Côte d’Azur, Centre National de la Recherche Scientifique, Institut de Pharmacologie Moléculaire et Cellulaire, Labex ICST)
- Dahui Li
(The University of Hong Kong)
- Yue Shi
(Xi’an Jiaotong University Health Science Center, Key Laboratory of Environment and Genes Related to Diseases)
- Sabrina Kurz
(Max Planck Institute for Heart and Lung Research, Department of Pharmacology)
- Jiong Hu
(Goethe University)
- Lei Wang
(Max Planck Institute for Heart and Lung Research, Department of Pharmacology)
- Jingchen Shao
(Max Planck Institute for Heart and Lung Research, Department of Pharmacology)
- Ann Atzberger
(Flow Cytometry Service Group)
- Zheng Wang
(First Affiliated Hospital of Xi’an Jiaotong University)
- Changhe Wang
(Xi’an Jiaotong University)
- Weijin Zang
(Xi’an Jiaotong University Health Science Center)
- Ingrid Fleming
(Goethe University)
- Nina Wettschureck
(Max Planck Institute for Heart and Lung Research, Department of Pharmacology
Goethe University Frankfurt)
- Eric Honoré
(Université Côte d’Azur, Centre National de la Recherche Scientifique, Institut de Pharmacologie Moléculaire et Cellulaire, Labex ICST)
- Stefan Offermanns
(Max Planck Institute for Heart and Lung Research, Department of Pharmacology
Goethe University Frankfurt)
Abstract
White adipose tissue (WAT) expansion in obesity occurs through enlargement of preexisting adipocytes (hypertrophy) and through formation of new adipocytes (adipogenesis). Adipogenesis results in WAT hyperplasia, smaller adipocytes and a metabolically more favourable form of obesity. How obesogenic WAT hyperplasia is induced remains, however, poorly understood. Here, we show that the mechanosensitive cationic channel Piezo1 mediates diet-induced adipogenesis. Mice lacking Piezo1 in mature adipocytes demonstrated defective differentiation of preadipocyte into mature adipocytes when fed a high fat diet (HFD) resulting in larger adipocytes, increased WAT inflammation and reduced insulin sensitivity. Opening of Piezo1 in mature adipocytes causes the release of the adipogenic fibroblast growth factor 1 (FGF1), which induces adipocyte precursor differentiation through activation of the FGF-receptor-1. These data identify a central feed-back mechanism by which mature adipocytes control adipogenesis during the development of obesity and suggest Piezo1-mediated adipocyte mechano-signalling as a mechanism to modulate obesity and its metabolic consequences.
Suggested Citation
ShengPeng Wang & Shuang Cao & Malika Arhatte & Dahui Li & Yue Shi & Sabrina Kurz & Jiong Hu & Lei Wang & Jingchen Shao & Ann Atzberger & Zheng Wang & Changhe Wang & Weijin Zang & Ingrid Fleming & Nina, 2020.
"Adipocyte Piezo1 mediates obesogenic adipogenesis through the FGF1/FGFR1 signaling pathway in mice,"
Nature Communications, Nature, vol. 11(1), pages 1-13, December.
Handle:
RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-16026-w
DOI: 10.1038/s41467-020-16026-w
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