ID | 118940 |
Author |
Dong, Bingzi
Tokushima University|Qingdao University
Hiasa, Masahiro
Tokushima University
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Higa, Yoshiki
Tokushima University
Ohnishi, Yukiyo
Tokushima University
Endo, Itsuro
Tokushima University
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Takashi, Yuichi
Tokushima University
Tsoumpra, Maria
Tokushima University
Kainuma, Risa
Tokushima University|Setsuro Tech Inc.
Sawatsubashi, Shun
Tokushima University
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Kiyonari, Hiroshi
RIKEN
Shioi, Go
RIKEN
Sakaue, Hiroshi
Tokushima University
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Nakashima, Tomoki
Tokyo Medical and Dental University
Kato, Shigeaki
Fukushima Medical University
Abe, Masahiro
Tokushima University
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Content Type |
Journal Article
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Description | Exercise results in mechanical loading of the bone and stimulates energy expenditure in the adipose tissue. It is therefore likely that the bone secretes factors to communicate with adipose tissue in response to mechanical loading. Interleukin (IL)−11 is known to be expressed in the bone, it is upregulated by mechanical loading, enhances osteogenesis and suppresses adipogenesis. Here, we show that systemic IL-11 deletion (IL-11−/−) results in reduced bone mass, suppressed bone formation response to mechanical loading, enhanced expression of Wnt inhibitors, and suppressed Wnt signaling. At the same time, the enhancement of bone resorption by mechanical unloading was unaffected. Unexpectedly, IL-11−/− mice have increased systemic adiposity and glucose intolerance. Osteoblast/osteocyte-specific IL-11 deletion in osteocalcin-Cre;IL-11fl/fl mice have reduced serum IL-11 levels, blunted bone formation under mechanical loading, and increased systemic adiposity similar to IL-11−/− mice. Adipocyte-specific IL-11 deletion in adiponectin-Cre;IL-11fl/fl did not exhibit any abnormalities. We demonstrate that osteoblast/osteocyte-derived IL-11 controls both osteogenesis and systemic adiposity in response to mechanical loading, an important insight for our understanding of osteoporosis and metabolic syndromes.
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Journal Title |
Nature Communications
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ISSN | 20411723
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NCID | AA12645905
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Publisher | Springer Nature
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Volume | 13
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Start Page | 7194
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Published Date | 2022-11-23
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Rights | This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
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DOI (Published Version) | |
URL ( Publisher's Version ) | |
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language |
eng
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TextVersion |
Publisher
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departments |
Oral Sciences
Medical Sciences
University Hospital
Institute of Advanced Medical Sciences
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