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Bone Abstracts (2013) 1 PP39 | DOI: 10.1530/boneabs.1.PP39

ECTS2013 Poster Presentations Bone biomechanics and quality (28 abstracts)

Glucose-dependent insulinotropic polypeptide receptor deletion results in a reduced bone strength and quality

Aleksandra Mieczkowska 1 , Nigel Irwin 2 , Peter R Flatt 2 , Daniel Chappard 1 & Guillaume Mabilleau 1

1LUNAM Université, Angers, France; 2University of Ulster, Coleraine, UK.

Objectives: Glucose-dependent insulinotropic polypeptide (GIP) is secreted by intestinal K-cells into the blood supply in response to nutrient ingestion and absorption. Although osteoblasts and osteoclasts express the GIP receptor (GIPR), the main action of the GIP/GIPR pathway in bone physiology and bone quality is unknown. The aim of the present study was to investigate bone quality in a mouse model of GIPR deficiency.

Materials/methods: Eleven 16 weeks old GIPR knock-out male mice, with a deletion of the first six exons of the GIPRr gene, were age- and sex-matched with 12 wild-type (WT) mice for this study. Resistance to fracture was studied by three-point bending in femur, whilst cortical microarchitecture was determined by high resolution microCT and quantitative X-ray imaging. Intrinsic material properties were investigated by nanoindentation. In addition, bone mineral and collagen properties were assessed by quantitative backscattered electron imaging (qBEI) and Fourier-transformed infrared microscopy (FTIRM). Non-parametric Mann–Whitney U test was used to compare differences between groups.

Results: As compared with control mice, GIPR KO animals presented a reduction in bone strength as evidenced by significant decreases in ultimate load (−11%) and absorbed energy (−28%). Cortical microarchitecture was also affected by the lack of a functional GIPR as demonstrated by significant reductions in cortical thickness (−20%) and cross-sectional moment of inertia (−18%). These microarchitectural modifications were accompanied by alterations of intrinsic material properties. Indeed maximal load and hardness as assessed by nanoindentation on hydrated bone were significantly reduced by 13 and 16% respectively. Furthermore, bone mineral density distribution was also decreased by 12% and the ratio of mature/immature collagen cross-links was reduced by 16%.

Conclusion: The inactivation of the GIP/GIPR pathway resulted in marked alterations of cortical microarchitecture, bone matrix properties and bone strength. Overall, these data support a fundamental role of the GIP/GIPR pathway in bone physiology.

Volume 1

European Calcified Tissue Society Congress 2013

Lisbon, Portugal
18 May 2013 - 22 May 2013

European Calcified Tissue Society 

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