The GDF11-FTO-PPARγ axis controls the shift of osteoporotic MSC fate to adipocyte and inhibits bone formation during osteoporosis.

During osteoporosis, the shift of bone mesenchymal stem cell (BMSC) lineage commitment to adipocyte leads to the imbalance between bone mass and fat, which increases the risk of fracture. The mechanism underlying this process is not fully understood. Fat mass and obesity-associated protein (FTO) is an RNA demethylase that demethylates various methylated nucleic acids and participates in various physiological and pathological processes.

Local bone interaction between renin-angiotensin system and kallikrein-kinin system in diabetic rat.

Objective: This study was performed to investigate bone deteriorations and the involvement of skeletal renin-angiotensin system (RAS) and kallikrein-kinin system (KKS) of male rat in response to the hyperglycemia.

Methods: The biomarkers in serum and urine were measured by ELISA kit, and tibias were taken for the measurement on gene, protein expression and histological analysis, femurs were taken for the measurement on biomechanical parameters and micro-CT.

Results: The DM1 showed the decreased level of osteocalcin, testosterone and FGF-23, and the increased level of serum CTX as compared to those of vehicle group.

Cigarette smoking and risk of hip fracture in women: a meta-analysis of prospective cohort studies.

Background And Objectives: Whether cigarette smoking can increase the risk of hip fracture in women is unclear. This meta-analysis, which pooled results from 10 prospective cohort studies, was performed to derive a more precise estimation between cigarette smoking and the risk of hip fracture in women.

Materials And Methods: Pubmed, Cochrane Central Register of Controlled Trials and ISI Web of Science were systematically searched to identify relevant studies.

Hepcidin1 knockout mice display defects in bone microarchitecture and changes of bone formation markers.

Iron accumulation is a risk factor of osteoporosis; mechanisms leading to iron-related bone loss are not fully determined. We sought to better understand the effect of chronic iron accumulation on bone over the life span in a mouse model. Hepcidin1 knockout (Hepc1(-/-)) male mice and their littermate control wild type (WT) mice at 7 months old were used in this study.