Age-related bone loss: lessons from the osteoporotic SAMP6 mouse model

摘要: Abstract SAMP6 mice exhibit features of skeletal aging including reduced bone mineral density (BMD), diminished rate formation, fewer mesenchymal stem cell (MSC) progenitors osteoblasts, decreased osteoblasts and increased marrow adipocytes. A decrease in the self-renewal capacity MSCs may account for osteoblast number formation. Increased activation, or overexpression, transcription factor PPARγ2 also contribute as phenotype were reproduced by feeding ligand rosiglitazone to normal mice. Genetic mapping studies utilizing F2 progeny mated with either SAMR1 related AKR/J strain identified quantitative trait loci (QTLs) vertebral BMD on chromosomes 2, 7, 11, 13, 16, 18, X. Transfer AKR allele chromosome 2 QTL into backcrossing caused a 5.0–5.4% increase BMD, accounting ∼50% difference between AKR/J. Studies Scottish postmenopausal women revealed an association X locus thus demonstrating applicability information derived from humans. Future genetic functional should therefore provide clues why production is during