By contrast, these traits are broadly dysregulated in bones following menopause and in patients with obesity or diseases such as chronic inflammation and cancer, where the loss of adiponectin, or changes in environmental cues that impact the downstream signalling pathways triggered by adiponectin (e.g. MAPK vs AMPK) pathologically tip the balance in favour of bone resorption and damage (Fig. 3). The gene discussed is ADIPOQ; the disease is obesity due to melanocortin 4 receptor deficiency.