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Bone Abstracts (2014) 3 PP86 | DOI: 10.1530/boneabs.3.PP86

Bone development/growth and fracture repair

Circulating myostatin in type 2 diabetes subjects: relationship with bone metabolism and fractures

Rebeca Reyes-Garcia1,2, Antonia Garcia-Martin1,3, Beatriz Garcia-Fontana1, Sonia Morales-Santana1,4, Pedro Rozas-Moreno1,5 & Manuel Muñoz-Torres1

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1Bone Metabolic Unit (RETICEF), Endocrinology Division, Instituto de Investigación de Granada, Hospital Universitario San Cecilio, Granada, Spain; 2Endocrinology Unit. Hospital General Universitario Rafael Mendez, Lorca, Murcia, Spain; 3Endocrinology Hospital Comarcal del Noroeste, Caravaca de la Cruz, Murcia, Spain; 4Proteomic Research Service, Fundación para la Investigación Biosanitaria de Andalucía Oriental -Alejandro Otero- (FIBAO), Granada, Spain; 5Endocrinology Division, Hospital General de Ciudad Real, Ciudad Real, Spain.


Introduction: Myostatin (growth differentiation factor 8, GDF-8) has an important role in the regulation of muscle mass, and mice lacking the myostatin gene show a generalized increase in bone density and strength. Type 2 diabetes subjects have an increased risk of fragility fractures despite of higher bone mass. Taking into account the myostatin influence in bone strength a better understanding of myostatin actions in type 2 diabetes is of interest.

Objectives: Our aims were to evaluate serum myostatin concentrations in type 2 diabetes patients, and to explore its relationship with bone mineral density (BMD), bone turnover markers and fractures.

Methods: Our study was a cross-sectional one including 73 type 2 diabetes patients. Concentrations of myostatin were measured by ELISA (R&D systems). BMD was evaluated by DXA (Hologic QDR 4500).

Results: Mean age was 56±6 years and duration of diabetes was 13±7 years. Serum myostatin showed no correlation with BMD at lumbar spine (r=0.074), femoral neck (r=0.130), or total hip (r=0.174), P>0.05 for all. Moreover, there was no relationship with bone turnover markers: OC: r=0.080; BSAP: r=0.150; TRAP: r=0.027; CTX: r=0.001, P>0.05 for all. Finally, myostatin showed no differences according to the presence of prevalent fractures: fractures 2800±1309 pg/ml vs no fractures 2542±957 pg/ml, P=0.372.

Conclusion: Our data does not support an association between serum myostatin and bone parameters in type 2 diabetes. A true lack of relationship in humans may be an explanation, although a disrupted regulation of this pathway in type 2 diabetes may also take place.

Volume 3

European Calcified Tissue Society Congress 2014

Prague, Czech Republic
17 May 2014 - 20 May 2014

European Calcified Tissue Society 

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