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Cited by 284

The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.

Regulation of bone formation by adiponectin through autocrine/paracrine and endocrine pathways

Open access
Shinoda, Yusuke, Yamaguchi, Masayuki, Ogata, Naoshi, Akune, Toru, Kubota, Naoto, Yamauchi, Toshimasa, Terauchi, Yasuo, Kadowaki, Takashi, Takeuchi, Yasuhiro, Fukumoto, Seiji, Ikeda, Toshiyuki, Hoshi, Kazuto, Chung, Ung‐il, Nakamura, Kozo, Kawaguchi, Hiroshi·2006·Journal of Cellular Biochemistry
DOI 10.1002/jcb.20890
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Abstract

Since interaction between bone and lipid metabolism has been suggested, this study investigated the regulation of bone metabolism by adiponectin, a representative adipokine, by analyzing deficient and overexpressing transgenic mice. We initially confirmed that adiponectin and its receptors were expressed in osteoblastic and osteoclastic cells, indicating that adiponectin can act on bone not only through an endocrine pathway as a hormone secreted from fat tissue, but also through an autocrine/paracrine pathway. There was no abnormality in bone mass or turnover of adiponectin‐deficient (Ad−/−) mice, possibly due to an equivalent balance of the two pathways. In the culture of bone marrow cells from the Ad−/− mice, osteogenesis was decreased compared to the wild‐type (WT) cell culture, indicating a positive effect of endogenous adiponectin through the autocrine/paracrine pathway. To examine the endocrine action of adiponectin, we analyzed transgenic mice overexpressing adiponectin in the liver, and found no abnormality in the bone. Addition of recombinant adiponectin in cultured osteoprogenitor cells suppressed osteogenesis, suggesting that the direct action of circulating adiponectin was negative for bone formation. In the presence of insulin, however, this suppression was blunted, and adiponectin enhanced the insulin‐induced phosphorylations of the main downstream molecule insulin receptor substrate‐1 and Akt. These lines of results suggest three distinct adiponectin actions on bone formation: a positive action through the autocrine/paracrine pathway by locally produced adiponectin, a negative action through the direct pathway by circulating adiponectin, and a positive action through the indirect pathway by circulating adiponectin via enhancement of the insulin signaling. J. Cell. Biochem. © 2006 Wiley‐Liss, Inc.

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Metadata

Authors
Shinoda, Y., Yamaguchi, M., Ogata, N., Akune, T., Kubota, N., Yamauchi, T., Terauchi, Y., Kadowaki, T., Takeuchi, Y., Fukumoto, S., Ikeda, T., Hoshi, K., Chung, U., Nakamura, K., & Kawaguchi, H.
Venue
Journal of Cellular Biochemistry
Publisher
Wiley
Published
2006-04-05
Volume
99
Issue
1
Pages
196-208
ISSN
  • 0730-2312 (ISSN-L)
  • 1097-4644
DOI
10.1002/jcb.20890
OpenAlex
W2168015812
Cited by
284
References
51
FWCI
5.65
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Regulation of bone formation by adiponectin through autocrine/paracrine and endocrine pathways. https://app.cochat.ai/papers/10.1002/jcb.20890
The paper
Shinoda, Y., Yamaguchi, M., Ogata, N., Akune, T., Kubota, N., Yamauchi, T., Terauchi, Y., Kadowaki, T., Takeuchi, Y., Fukumoto, S., Ikeda, T., Hoshi, K., Chung, U., Nakamura, K., & Kawaguchi, H. (2006). Regulation of bone formation by adiponectin through autocrine/paracrine and endocrine pathways. Journal of Cellular Biochemistry. https://doi.org/10.1002/jcb.20890

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.