Influence of adipokines and ghrelin on bone mineral density and fracture risk
Adipose tissue may regulate bone metabolism and be involved in osteoporosis pathophysiology. Adiponectin and leptin are adipokine hormones, synthesized by adipocytes. Leptin plays a particular role in weight and appetite regulation. Adiponectin regulates metabolism and inflammatory pathways. Ghrelin is a growth hormone secretagogue implicated in fat mass and appetite regulation. Epidemiological data have established positive relationships between fat mass and bone mineral density (BMD). Using systematic review and meta-analysis, the authors of this study [1] tested the association and correlation of adipokines (adiponectin, leptin) and ghrelin serum level with bone mineral density and fracture risk.
DLK1 is a novel regulator of bone mass that mediates estrogen deficiency-induced bone loss
DLK1 is a transmembrane protein that acts as a membrane-bound or soluble protein to regulate regeneration of a number of adult tissues. Several lines of evidence suggest an important role of DLK1 in skeletal development and function. The aim of this paper [1] was to examine the role of this protein in bone biology using osteoblast specific DLK1 overexpressing mice (Col-Dlk1).
Adipokines and the risk of fracture in older adults
Adiponectin and leptin, two adipokines, have been shown to influence bone metabolism in vitro and in animal models, and they have been associated with bone mineral density (BMD). Little is known about the association between leptin and adiponectin serum levels and the fracture risk. The authors of a recent study [1] tested the hypothesis that low leptin and high adiponectin levels are each individually associated with increased fracture risk in a prospective cohort study, among 3075 elderly men and women.
Use of antidepressant drugs and risk of osteoporotic and nonosteoporotic fractures
The antidepressant classes selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressant drugs (TCAs) have been associated with increased risk of fractures.
Serum fibroblast growth factor-23 (FGF-23) and fracture risk in elderly men
Since the population in the developed world is aging, the burden of fragility fractures is a constantly increasing problem. Potent bone-specific pharmaceutical agents have become available. However, the identification of patients with a high risk of bone fractures, who will benefit from these agents, remains an important challenge. Fibroblast growth factor 23 (FGF-23) is a circulating factor expressed predominantly in osteoblasts and osteocytes that negatively regulates serum levels of inorganic phosphate (Pi) and 1,25-dihydroxy-vitamin D3. Overexpression of FGF-23 in transgenic mice led to demineralization and renal phosphate leakage. Accordingly, diseases resulting in high circulating FGF-23 concentration, such as autosomic dominant hypophosphatemic rickets (which is due to stabilizing mutations in the FGF-23 gene) or tumor-induced osteomalacia (which is the consequence of FGF-23 secretion by certain tumors) are associated with generalized osteomalacia, skeletal deformities, and a high risk of fractures. FGF-23 is not, however, associated with reduced bone mineral density in the general population. Whether or not high serum FGF-23 concentrations correlate with an increased risk of fracture in the general population is unknown.
 Download here the slide set presented by Prof. Friedlander, on Thursday, November 10th. |
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