Osteoblast/osteocyte-derived interleukin-11 regulates osteogenesis and systemic adipogenesis

Bingzi Dong, Masahiro Hiasa, Yoshiki Higa, Yukiyo Ohnishi, Itsuro Endo, Takeshi Kondo, Yuichi Takashi, Maria Tsoumpra, Risa Kainuma, Shun Sawatsubashi, Hiroshi Kiyonari, Go Shioi, Hiroshi Sakaue, Tomoki Nakashima, Shigeaki Kato, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto ()
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Bingzi Dong: Tokushima University
Masahiro Hiasa: Tokushima University Graduate School of Dentistry
Yoshiki Higa: Tokushima University Graduate School of Dentistry
Yukiyo Ohnishi: Tokushima University Graduate School of Medical Sciences
Itsuro Endo: Tokushima University Graduate School of Medical Sciences
Takeshi Kondo: Tokushima University Graduate School of Medical Sciences
Yuichi Takashi: Tokushima University
Maria Tsoumpra: Tokushima University
Risa Kainuma: Tokushima University
Shun Sawatsubashi: Tokushima University
Hiroshi Kiyonari: RIKEN Center for Biosystems Dynamics Research
Go Shioi: RIKEN Center for Biosystems Dynamics Research
Hiroshi Sakaue: Tokushima University Graduate School of Nutritional Sciences
Tomoki Nakashima: Tokyo Medical and Dental University
Shigeaki Kato: Fukushima Medical University
Masahiro Abe: Tokushima University Graduate School of Medical Sciences
Seiji Fukumoto: Tokushima University
Toshio Matsumoto: Tokushima University

Nature Communications, 2022, vol. 13, issue 1, 1-17

Abstract: Abstract 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.

Date: 2022
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DOI: 10.1038/s41467-022-34869-3

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