Enteroendocrine K Cells Exert Complementary Effects to Control Bone Quality and Mass in Mice

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Standard

Enteroendocrine K Cells Exert Complementary Effects to Control Bone Quality and Mass in Mice. / Gobron, Benoit; Bouvard, Beatrice; Vyavahare, Sagar; Blom, Liv V. V.; Pedersen, Kristian K.; Windelov, Johanne A.; Boer, Geke A.; Harada, Norio; Zhang, Sheng; Shimazu-Kuwahara, Satoko; Wice, Burton; Inagaki, Nobuya; Legrand, Erick; Flatt, Peter R.; Chappard, Daniel; Hartmann, Bolette; Holst, Jens J.; Rosenkilde, Mette M.; Irwin, Nigel; Mabilleau, Guillaume.

I: Journal of Bone and Mineral Research, Bind 35, Nr. 7, 2020, s. 1363-1374.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Gobron, B, Bouvard, B, Vyavahare, S, Blom, LVV, Pedersen, KK, Windelov, JA, Boer, GA, Harada, N, Zhang, S, Shimazu-Kuwahara, S, Wice, B, Inagaki, N, Legrand, E, Flatt, PR, Chappard, D, Hartmann, B, Holst, JJ, Rosenkilde, MM, Irwin, N & Mabilleau, G 2020, 'Enteroendocrine K Cells Exert Complementary Effects to Control Bone Quality and Mass in Mice', Journal of Bone and Mineral Research, bind 35, nr. 7, s. 1363-1374. https://doi.org/10.1002/jbmr.4004

APA

Gobron, B., Bouvard, B., Vyavahare, S., Blom, L. V. V., Pedersen, K. K., Windelov, J. A., Boer, G. A., Harada, N., Zhang, S., Shimazu-Kuwahara, S., Wice, B., Inagaki, N., Legrand, E., Flatt, P. R., Chappard, D., Hartmann, B., Holst, J. J., Rosenkilde, M. M., Irwin, N., & Mabilleau, G. (2020). Enteroendocrine K Cells Exert Complementary Effects to Control Bone Quality and Mass in Mice. Journal of Bone and Mineral Research, 35(7), 1363-1374. https://doi.org/10.1002/jbmr.4004

Vancouver

Gobron B, Bouvard B, Vyavahare S, Blom LVV, Pedersen KK, Windelov JA o.a. Enteroendocrine K Cells Exert Complementary Effects to Control Bone Quality and Mass in Mice. Journal of Bone and Mineral Research. 2020;35(7):1363-1374. https://doi.org/10.1002/jbmr.4004

Author

Gobron, Benoit ; Bouvard, Beatrice ; Vyavahare, Sagar ; Blom, Liv V. V. ; Pedersen, Kristian K. ; Windelov, Johanne A. ; Boer, Geke A. ; Harada, Norio ; Zhang, Sheng ; Shimazu-Kuwahara, Satoko ; Wice, Burton ; Inagaki, Nobuya ; Legrand, Erick ; Flatt, Peter R. ; Chappard, Daniel ; Hartmann, Bolette ; Holst, Jens J. ; Rosenkilde, Mette M. ; Irwin, Nigel ; Mabilleau, Guillaume. / Enteroendocrine K Cells Exert Complementary Effects to Control Bone Quality and Mass in Mice. I: Journal of Bone and Mineral Research. 2020 ; Bind 35, Nr. 7. s. 1363-1374.

Bibtex

@article{5e505607b8f04dac825606dbec459a7a,
title = "Enteroendocrine K Cells Exert Complementary Effects to Control Bone Quality and Mass in Mice",
abstract = "The involvement of a gut-bone axis in controlling bone physiology has been long suspected, although the exact mechanisms are unclear. We explored whether glucose-dependent insulinotropic polypeptide (GIP)-producing enteroendocrine K cells were involved in this process. The bone phenotype of transgenic mouse models lacking GIP secretion (GIP-GFP-KI) or enteroendocrine K cells (GIP-DT) was investigated. Mice deficient in GIP secretion exhibited lower bone strength, trabecular bone mass, trabecular number, and cortical thickness, notably due to higher bone resorption. Alterations of microstructure, modifications of bone compositional parameters, represented by lower collagen cross-linking, were also apparent. None of these alterations were observed in GIP-DT mice lacking enteroendocrine K cells, suggesting that another K-cell secretory product acts to counteract GIP action. To assess this, stable analogues of the known K-cell peptide hormones, xenin and GIP, were administered to mature NIH Swiss male mice. Both were capable of modulating bone strength mostly by altering bone microstructure, bone gene expression, and bone compositional parameters. However, the two molecules exhibited opposite actions on bone physiology, with evidence that xenin effects are mediated indirectly, possibly via neural networks. Our data highlight a previously unknown interaction between GIP and xenin, which both moderate gut-bone connectivity. (c) 2020 American Society for Bone and Mineral Research.",
keywords = "BONE REMODELING, ENTEROENDOCRINE SYSTEM, GIP, XENIN, GASTRIC-INHIBITORY POLYPEPTIDE, GLUCAGON-LIKE PEPTIDE-1, NEUROTENSIN RECEPTOR, INSULIN-RESISTANCE, ACETYLCHOLINE, EXPRESSION, OSTEOBLAST, SECRETION, REDUCTION",
author = "Benoit Gobron and Beatrice Bouvard and Sagar Vyavahare and Blom, {Liv V. V.} and Pedersen, {Kristian K.} and Windelov, {Johanne A.} and Boer, {Geke A.} and Norio Harada and Sheng Zhang and Satoko Shimazu-Kuwahara and Burton Wice and Nobuya Inagaki and Erick Legrand and Flatt, {Peter R.} and Daniel Chappard and Bolette Hartmann and Holst, {Jens J.} and Rosenkilde, {Mette M.} and Nigel Irwin and Guillaume Mabilleau",
year = "2020",
doi = "10.1002/jbmr.4004",
language = "English",
volume = "35",
pages = "1363--1374",
journal = "Journal of Bone and Mineral Research",
issn = "0884-0431",
publisher = "Wiley-Blackwell",
number = "7",

}

RIS

TY - JOUR

T1 - Enteroendocrine K Cells Exert Complementary Effects to Control Bone Quality and Mass in Mice

AU - Gobron, Benoit

AU - Bouvard, Beatrice

AU - Vyavahare, Sagar

AU - Blom, Liv V. V.

AU - Pedersen, Kristian K.

AU - Windelov, Johanne A.

AU - Boer, Geke A.

AU - Harada, Norio

AU - Zhang, Sheng

AU - Shimazu-Kuwahara, Satoko

AU - Wice, Burton

AU - Inagaki, Nobuya

AU - Legrand, Erick

AU - Flatt, Peter R.

AU - Chappard, Daniel

AU - Hartmann, Bolette

AU - Holst, Jens J.

AU - Rosenkilde, Mette M.

AU - Irwin, Nigel

AU - Mabilleau, Guillaume

PY - 2020

Y1 - 2020

N2 - The involvement of a gut-bone axis in controlling bone physiology has been long suspected, although the exact mechanisms are unclear. We explored whether glucose-dependent insulinotropic polypeptide (GIP)-producing enteroendocrine K cells were involved in this process. The bone phenotype of transgenic mouse models lacking GIP secretion (GIP-GFP-KI) or enteroendocrine K cells (GIP-DT) was investigated. Mice deficient in GIP secretion exhibited lower bone strength, trabecular bone mass, trabecular number, and cortical thickness, notably due to higher bone resorption. Alterations of microstructure, modifications of bone compositional parameters, represented by lower collagen cross-linking, were also apparent. None of these alterations were observed in GIP-DT mice lacking enteroendocrine K cells, suggesting that another K-cell secretory product acts to counteract GIP action. To assess this, stable analogues of the known K-cell peptide hormones, xenin and GIP, were administered to mature NIH Swiss male mice. Both were capable of modulating bone strength mostly by altering bone microstructure, bone gene expression, and bone compositional parameters. However, the two molecules exhibited opposite actions on bone physiology, with evidence that xenin effects are mediated indirectly, possibly via neural networks. Our data highlight a previously unknown interaction between GIP and xenin, which both moderate gut-bone connectivity. (c) 2020 American Society for Bone and Mineral Research.

AB - The involvement of a gut-bone axis in controlling bone physiology has been long suspected, although the exact mechanisms are unclear. We explored whether glucose-dependent insulinotropic polypeptide (GIP)-producing enteroendocrine K cells were involved in this process. The bone phenotype of transgenic mouse models lacking GIP secretion (GIP-GFP-KI) or enteroendocrine K cells (GIP-DT) was investigated. Mice deficient in GIP secretion exhibited lower bone strength, trabecular bone mass, trabecular number, and cortical thickness, notably due to higher bone resorption. Alterations of microstructure, modifications of bone compositional parameters, represented by lower collagen cross-linking, were also apparent. None of these alterations were observed in GIP-DT mice lacking enteroendocrine K cells, suggesting that another K-cell secretory product acts to counteract GIP action. To assess this, stable analogues of the known K-cell peptide hormones, xenin and GIP, were administered to mature NIH Swiss male mice. Both were capable of modulating bone strength mostly by altering bone microstructure, bone gene expression, and bone compositional parameters. However, the two molecules exhibited opposite actions on bone physiology, with evidence that xenin effects are mediated indirectly, possibly via neural networks. Our data highlight a previously unknown interaction between GIP and xenin, which both moderate gut-bone connectivity. (c) 2020 American Society for Bone and Mineral Research.

KW - BONE REMODELING

KW - ENTEROENDOCRINE SYSTEM

KW - GIP

KW - XENIN

KW - GASTRIC-INHIBITORY POLYPEPTIDE

KW - GLUCAGON-LIKE PEPTIDE-1

KW - NEUROTENSIN RECEPTOR

KW - INSULIN-RESISTANCE

KW - ACETYLCHOLINE

KW - EXPRESSION

KW - OSTEOBLAST

KW - SECRETION

KW - REDUCTION

U2 - 10.1002/jbmr.4004

DO - 10.1002/jbmr.4004

M3 - Journal article

C2 - 32155286

VL - 35

SP - 1363

EP - 1374

JO - Journal of Bone and Mineral Research

JF - Journal of Bone and Mineral Research

SN - 0884-0431

IS - 7

ER -

ID: 247546175