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. Author manuscript; available in PMC: 2013 May 22.
Published in final edited form as: Nat Rev Rheumatol. 2009 May 26;5(7):365–372. doi: 10.1038/nrrheum.2009.102

Figure 3.

Figure 3

Leptin signaling via the hypothalamus to the SNS/b-adrenergic receptors in osteoblasts triggers bone loss, but putative direct anabolic leptin effects on osteoblasts remain unresolved. Osteocalcin produced by osteoblasts decreases fat mass, promotes adiponectin production and insulin sensitivity, and increases pancreating b-cell mass and insulin secretion. Adipose-derived PPARg2 promotes marrow adiposity and decreases bone mass. Potential therapeutic targets include b-adrenergic blockade to reduce leptin-induced bone loss, recombinant leptin or leptin mimetic to increase bone mass, PPARg agonism/antagonism to inhibit marrow adiposity and increase osteoblast differentiation, and recombinant osteocalcin or g-carboxylation inhibitors to inhibit adipose deposition and improve bone mass.