The importance of coordinating whole body energy balance is known, however, the mechanism controlling and integrating the energy homeostasis of individual tissues during weight change is unclear. Employing transcriptomic and proteomic analysis of Y1 receptor deficient osteoblasts combined with the generation of a genetically modified mouse model we have identified a novel circuitry that is responsible for coordinating bone accretion with changes in energy balance and identify the NPY controlled release of osteoglycin from osteoblasts as the critical component. Osteoglycin acts to suppress bone formation when energy levels are low and to modulate whole body energy supplies by altering glucose uptake through changes in insulin secretion and sensitivity, as well as by altering food intake through central signalling. Human studies show that osteoglycin is associated with BMI and lean mass as well as changes in weight, BMI and glucose levels as a result of the negative energy balance elicited by gastric surgery. Thus, we identify osteoglycin as a novel factor facilitating matching of bone acquisition to alterations in energy status.