Both spontaneous Ins2+/− and streptozotocin‐induced type I diabetes cause bone loss in young mice12. Issue 4 (20th December 2012)

• Record Type: Journal Article
• Authors: Coe, Lindsay M.; Zhang, Jing; McCabe, Laura R.
• Is Part Of: Journal of cellular physiology. Volume 228:Issue 4(2013:Apr.)
• Page Start: 689
• Page End: 695
• Publication Date: 2012-12-20
• Subjects: Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.24177
• Languages: English
• ISSNs: 0021-9541

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <p>The adolescent skeleton undergoes accelerated growth determining overall bone density, length, and quality. Diseases such as type 1 diabetes (T1D), most often diagnosed in adolescents, can alter bone processes and promote bone loss. Studies examining type 1 diabetic (T1D) bone pathologies typically utilize adult mice and rely on pharmacologic models such as streptozotocin (STZ)‐induced diabetic rodents. To test the effect of T1D on adolescent bone growth/density we used a novel juvenile genetic model (<italic>Ins</italic>2<sup>+/−</sup> mice) that spontaneously develop T1D at approximately 5 weeks of age and compared our findings with STZ‐induced T1D mice. Compared to controls, both <italic>Ins</italic>2<sup>+/−</sup> and STZ‐induced T1D mice displayed blood glucose levels greater than 300 mg/dl and reduced body, fat and muscle mass as well as femur trabecular bone density. STZ mice exhibited greater bone loss compared to <italic>Ins</italic>2<sup>+/−</sup> mice despite having lower blood glucose levels. Cortical bone was affected in STZ but not <italic>Ins</italic>2<sup>+/−</sup> mice. Osteocalcin serum protein and bone RNA levels decreased in both models. Consistent with studies in adult mice, STZ adolescent mice displayed increased marrow adiposity, however this was not observed in the <italic>Ins</italic>2<sup>+/−</sup> mice. Reduced femur length, decreased growth plate thickness and decreased collagen II expression in both model simplies impaired cartilage formation. In summary, both pharmacologic and spontaneous adolescent T1D mice demonstrated a bone synthesis and growth defect. STZ appears to cause a more severe phenotype. Thus, the <italic>Ins2</italic><sup>+/−</sup> mouse could serve as a useful model to study adolescent T1D bone loss with fewer complications. J. Cell. Physiol. 228: 689–695, 2013. © 2012 Wiley Periodicals, Inc.</p> </abstract>