Bone remodeling, which is affected in osteoporosis, comprises two phases: bone formation by matrix-producing osteoblasts and bone resorption by osteoclasts. The demonstration that the anorexigenic hormone leptin inhibits bone formation through a hypothalamic relay suggests that other molecules that affect energy metabolism in the hypothalamus could also modulate bone mass. Neuromedin U is an anorexigenic neuropeptide that acts independently of leptin through poorly defined mechanisms.

A recent study [1] shows that neuromedin U-deficient mice have high bone mass owing to an increase in bone formation; this is more prominent in male mice than female mice. Physiological and cell-based assays indicate that neuromedin U acts in the central nervous system, rather than directly on bone cells, to regulate bone remodeling.
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