Streptozotocin, Type I Diabetes Severity and Bone
Bone remodeling
DOI:
10.1007/s12575-009-9000-5
Publication Date:
2009-08-11T20:04:20Z
AUTHORS (2)
ABSTRACT
As many as 50% of adults with type I (T1) diabetes exhibit bone loss and are at increased risk for fractures. Therapeutic development to prevent and/or restore lost in T1 diabetic patients requires knowledge the molecular mechanisms accounting pathology. Because cell culture models alone cannot fully address systemic/metabolic complexity diabetes, animal critical. A variety exist including spontaneous pharmacologically induced rodents. In this paper, we discuss streptozotocin (STZ)-induced mouse model examine dose-dependent effects on disease severity bone. Five daily injections either 40 or 60 mg/kg STZ induce pathologies similar spontaneously rat human Specifically, volume, mineral apposition rate, osteocalcin serum tibia messenger RNA levels decreased. contrast, marrow adiposity aP2 expression dose. However, high-dose caused a more rapid elevation blood glucose greater magnitude change body mass, fat pad gene (osteocalcin, aP2). An increase cathepsin K ratio RANKL/OPG was noted mice, suggesting possibility that severe could osteoclast activity, something not seen lower doses. This may contribute some disparity between existing studies regarding role osteoclasts Examination kidney liver toxicity indicate high dose causes inflammation. summary, multiple low-dose exhibits phenotype models, has low toxicity, serves useful tool examining loss.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (73)
CITATIONS (101)
EXTERNAL LINKS
PlumX Metrics
RECOMMENDATIONS
FAIR ASSESSMENT
Coming soon ....
JUPYTER LAB
Coming soon ....