The principal cellular constituents of bone (primarily osteoblasts and osteoclasts) rapidly respond to circulating signals, altering global levels of bone formation and resorption respectively, and thus impacting bone homeostasis.1–3 The effects of adiponectin in bone have been researched in multiple conditions;however, these studies report variable outcomes with little explanation. Further exploration of adiponectin signalling is essential to fully under-stand the possibility of promoting or inhibiting its actions during ageing or disease.