Abstract
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.
Highlights
Type 1 diabetes (T1D) is a metabolic disease, characterized by hypoinsulinemia and thyperglycemia that has profound effect on the bone [1,2]
We found that T1D caused bone loss in all strains, but the magnitude of bone loss was greatest in 129/Sv
To address the role of mouse genotype/strain on T1D bone pathology, we used the multiple low dose STZ injection method to induce T1D in Balb/c, C57BL/6 and 129/Sv mice, strains that are commonly used in research
Summary
Type 1 diabetes (T1D) is a metabolic disease, characterized by hypoinsulinemia and thyperglycemia that has profound effect on the bone [1,2]. Potential contributors to the pathogenesis of T1D bone loss include disturbed glucose metabolism [5,6] systemic and bone marrow inflammation [7,8,9], changes in lipid metabolism [10,11,12], and changes in systematic hormones [13] (Figure 1). Bone marrow adiposity, which can promote bone oss, may play less of a role in T1D osteoporosis [1,14,15], but is a key marker of the diabetic bone pathology in mice. The contribution of genetics in modifying the extent of T1D-induced bone loss has not been fully addressed
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