Mouse Strain Dependent and Independent Effects of Type 1 Diabetic Bone PathologyJing Zhang#, Lindsay Coe#, Katherine J Motyl and Laura R McCabe*
Departments of Physiology and Radiology, Michigan State University, USA
- *Corresponding Author:
- Laura R. McCabe
Departments of Physiology and Radiology
Michigan State University, 2201 Biomedical Physical Science Building
East Lansing, MI, USA, 48824
Tel: (517) 884-5152
Fax: (517) 355-5125
E-mail: [email protected]
Received date: July 27, 2012; Accepted date: September 16, 2012; Published date: September 22, 2012
Citation: Zhang J, Coe L, Motyl KJ, McCabe LR (2012) Mouse Strain Dependent and Independent Effects of Type 1 Diabetic Bone Pathology. J Diabetes Metab S1:008. doi: 10.4172/2155-6156.S1-008
Copyright: © 2012 Zhang J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Type 1 diabetes (T1D) contributes to bone loss in humans as well as in both spontaneous and pharmacologicinduced T1D mouse models. The severity of complications of T1D, such as nephropathy, differs in different mouse strains. However, the contribution of genetics in modifying the extent of T1D-induced bone loss has not been fully addressed. Here, we compare the T1D-induced bone pathology between three commonly used inbred mouse strains: Balb/c, C57BL/6 and 129/Sv mice. All T1D mouse strains displayed a characteristic bone phenotype characterized by significant bone loss, decreased levels of osteoblast markers and increased marrow adiposity. However, straindependent differences were also observed. Most notably, 129/Sv T1D mice displayed the greatest magnitude of bone loss despite having the least disease severity (as indicated by blood glucose levels) of the three strains studied. These findings suggest the contribution of strain dependent/genetically associated factors to the degree of bone loss observed in T1D mice.