Jing Zhang, Lindsay Coe, Katherine J Motyl and Laura R McCabe
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.
