Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice

A role for the gastro-intestinal tract in controlling bone remodeling is suspected since serum levels of bone remodeling markers are affected rapidly after a meal. Glucose-dependent insulinotropic polypeptide (GIP) represents a suitable candidate in mediating this effect. The aim of the present stud...

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Main Authors: Gaudin-Audrain, Christine, Irwin, Nigel, Mansur, Sity, Flatt, Peter R., Thorens, Bernard, Baslé, Michel, Chappard, Daniel, Mabilleau, Guillaume
Format: Article
Language:English
Published: Elsevier B.V. 2013
Subjects:
Online Access:http://eprints.uthm.edu.my/4785/1/AJ%202017%20%28638%29.pdf
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author Gaudin-Audrain, Christine
Irwin, Nigel
Mansur, Sity
Flatt, Peter R.
Thorens, Bernard
Baslé, Michel
Chappard, Daniel
Mabilleau, Guillaume
author_facet Gaudin-Audrain, Christine
Irwin, Nigel
Mansur, Sity
Flatt, Peter R.
Thorens, Bernard
Baslé, Michel
Chappard, Daniel
Mabilleau, Guillaume
author_sort Gaudin-Audrain, Christine
collection UTHM
description A role for the gastro-intestinal tract in controlling bone remodeling is suspected since serum levels of bone remodeling markers are affected rapidly after a meal. Glucose-dependent insulinotropic polypeptide (GIP) represents a suitable candidate in mediating this effect. The aim of the present study was to investigate the effect of total inhibition of GIP signaling on trabecular bone volume, microarchitecture and quality. We used GIP receptor (GIPR) knockout mice and investigated trabecular bone volume and microarchitecture by microCT and histomorphometry. GIPR-deficient animals at 16 weeks of age presented with a significant (20%) increase in trabecular bone mass accompanied by an increase (17%) in trabecular number. In addition, the number of osteoclasts and bone formation rate was significantly reduced and augmented, respectively in these animals when compared with wild-type littermates. These modifications of trabecular bone microarchitecture are linked to a remodeling in the expression pattern of adipokines in the GIPR-deficient mice. On the other hand, despite significant enhancement in bone volume, intrinsic mechanical properties of the bone matrix was reduced as well as the distribution of bone mineral density and the ratio of mature/immature collagen cross-links. Taken together, these results indicate an increase in trabecular bone volume in GIPR KO animals associated with a reduction in bone quality.
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spelling uthm.eprints-47852021-12-16T06:19:47Z http://eprints.uthm.edu.my/4785/ Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice Gaudin-Audrain, Christine Irwin, Nigel Mansur, Sity Flatt, Peter R. Thorens, Bernard Baslé, Michel Chappard, Daniel Mabilleau, Guillaume RC Internal medicine T Technology (General) A role for the gastro-intestinal tract in controlling bone remodeling is suspected since serum levels of bone remodeling markers are affected rapidly after a meal. Glucose-dependent insulinotropic polypeptide (GIP) represents a suitable candidate in mediating this effect. The aim of the present study was to investigate the effect of total inhibition of GIP signaling on trabecular bone volume, microarchitecture and quality. We used GIP receptor (GIPR) knockout mice and investigated trabecular bone volume and microarchitecture by microCT and histomorphometry. GIPR-deficient animals at 16 weeks of age presented with a significant (20%) increase in trabecular bone mass accompanied by an increase (17%) in trabecular number. In addition, the number of osteoclasts and bone formation rate was significantly reduced and augmented, respectively in these animals when compared with wild-type littermates. These modifications of trabecular bone microarchitecture are linked to a remodeling in the expression pattern of adipokines in the GIPR-deficient mice. On the other hand, despite significant enhancement in bone volume, intrinsic mechanical properties of the bone matrix was reduced as well as the distribution of bone mineral density and the ratio of mature/immature collagen cross-links. Taken together, these results indicate an increase in trabecular bone volume in GIPR KO animals associated with a reduction in bone quality. Elsevier B.V. 2013 Article PeerReviewed text en http://eprints.uthm.edu.my/4785/1/AJ%202017%20%28638%29.pdf Gaudin-Audrain, Christine and Irwin, Nigel and Mansur, Sity and Flatt, Peter R. and Thorens, Bernard and Baslé, Michel and Chappard, Daniel and Mabilleau, Guillaume (2013) Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice. BONE, 53 (NIL). pp. 221-230. ISSN 8756-3282 https://dx.doi.org/10.1016/j.bone.2012.11.039
spellingShingle RC Internal medicine
T Technology (General)
Gaudin-Audrain, Christine
Irwin, Nigel
Mansur, Sity
Flatt, Peter R.
Thorens, Bernard
Baslé, Michel
Chappard, Daniel
Mabilleau, Guillaume
Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice
title Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice
title_full Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice
title_fullStr Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice
title_full_unstemmed Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice
title_short Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice
title_sort glucose dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice
topic RC Internal medicine
T Technology (General)
url http://eprints.uthm.edu.my/4785/1/AJ%202017%20%28638%29.pdf
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