neuropeptide-y and Bone-Diseases

The metabolism and homeostasis of the skeletal system have historically been considered to be associated with the endocrine system. However, this view has been expanded with the recognition of several neural pathways playing important roles in the regulation of bone metabolism via central relays. In particular, bone metabolism and homeostasis have been reported to be precisely modulated by the central neural signaling. Initiated by the finding of leptin, the axis of neural regulation on bone expands rapidly. The semaphorin-plexin system plays an important role in the cross-talk between osteoclasts and osteoblasts; a complex system has also been identified and includes neuropeptide Y and cannabinoids. These findings facilitate our understanding of the central neuropeptides and neural factors in the modulation of bone metabolism and homeostasis, and these neuronal pathways also represent an area of research scenario that identifies the novel regulation between brain and bone. These regulatory mechanisms correlate with other homeostatic networks and demonstrate a more intricate and synergetic bone biology than previously envisioned. As such, this review summarizes the current knowledge of the neural regulation of bone metabolism and homeostasis, as well as its role in skeletal diseases and discusses the emerging challenges presented in this field.

Topics: Animals; Bone and Bones; Bone Diseases; Bone Remodeling; Brain; Homeostasis; Humans; Leptin; Neuropeptide Y; Semaphorins; Signal Transduction

In mice, neuropeptide Y (NPY) decreases bone turnover by means of a parathyroid hormone-independent effect on osteoblast activity.. Cross-sectional study.. We studied the relationship between levels of NPY and biomarkers of osteoblast activity in 161 nondiabetic patients with end-stage renal disease (131 patients, hemodialysis; 30 patients, continuous ambulatory peritoneal dialysis).. We performed an analysis of demographic and clinical variables associated with NPY as a dependent variable and a second analysis testing the association of NPY (as an independent variable) with markers of osteoblast activity.. Peritoneal dialysis as treatment modality (beta = 0.37; P < 0.001) and longer duration of dialysis therapy (beta = 0.24; P < 0.01) were independently related to plasma NPY. NPY level was related inversely (P < 0.001) to serum alkaline phosphatase and bone alkaline phosphatase levels (P = 0.01). The NPY-alkaline phosphatase link was confirmed in a multiple regression analysis adjusting for a series of potential confounders, including parathyroid hormone. In a categorical analysis in which the study population was divided according to NPY quartiles, the proportion of patients with low alkaline phosphatase levels was lowest in the first 2 NPY quartiles (26%) and highest in NPY quartile 4 (80%; P < 0.001), and this association held true in a multiple logistic regression analysis, indicating that the risk of low alkaline phosphatase level increases in parallel with NPY level.. The hypothesis generated by this cross-sectional study needs to be confirmed in cohort studies.. The inverse relationships between levels of NPY and biomarkers of bone turnover support the hypothesis that NPY may be implicated in low bone turnover in dialysis patients by a central parathyroid-independent mechanism.

Topics: Aged; Alkaline Phosphatase; Biomarkers; Bone and Bones; Bone Diseases; Cross-Sectional Studies; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Neuropeptide Y; Osteoblasts; Peritoneal Dialysis; Regression Analysis; Renal Dialysis