Hypothalamic control of bone formation: Distinct actions of leptin and Y2 receptor pathways

摘要: Leptin and Y2 receptors on hypothalamic NPY neurons mediate leptin effects energy homeostasis; however, their interaction in modulating osteoblast activity is not established. Here, direct testing of this possibility indicates distinct mechanisms action for anti-osteogenic Y2(-/-) anabolic pathways bone formation. Introduction: Central enhancement formation by observed leptin-deficient oblob receptor null mice. Similar elevation central neuropeptide Y (NPY) expression these two models suggest a shared pathway between the control physiology. The aim study was to test whether regulate same or mechanisms. Materials Methods: concomitant deficiency controlling examined double mutant mice, determine have additive effects. Interaction excess deletion using recombinant adeno-associated viral vector overproduction (AAV-NPY) produce weight gain thus adult Cancellous volume cell function were assessed. Results: Osteoblast comparably elevated oblob, Y2(-/-), However, greater resorption mice reduced cancellous compared with Y2(-/-). Both wildtype AAV-NPY exhibited marked white adipose tissue accumulation hence expression, thereby reducing activity. Despite effect obese model, remained significantly than Conclusions: This suggests that key regulator leptin-dependent activity, because both stimulation inhibition can occur presence high NPY. acts consistently stimulate formation; contrast, continues suppress as circulating levels increase. As result, they act increasingly opposition obesity becomes more marked. Thus, absence leptin, response loss be distinguished. increase physiological levels, signaling are revealed.