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. Author manuscript; available in PMC: 2016 Oct 25.
Published in final edited form as: Semin Nephrol. 2013 Mar;33(2):130–142. doi: 10.1016/j.semnephrol.2012.12.014

Figure 2.

Figure 2

Osteocalcin (Ocn)–GPRC6A bone endocrine networks. A complex network is depicted whereby undercarboxylated Ocn is released from bone in response to osteoclast-mediated bone resorption. Circulating Ocn targets a nutrient G-protein–coupled receptor, with high homology to CaSR, which is present in multiple organs, including pancreatic β-cells, adipocytes, skeletal muscle, hepatocytes, osteoblasts, Leydig cells in testes and prostate, as well as other tissues and cell types. Experimental evidence in the mouse suggests that Ocn is involved in regulating insulin secretion and insulin sensitivity as well as sexual reproduction through control of testosterone production in Leydig cells. Insulin may have a feed-forward loop to stimulate Ocn release from bone. Ocn regulation of testosterone may coordinate skeletal growth and sex hormone production during skeletal growth. The clinical significance of these pathways in human beings remains to be established. LH, luteinizing hormone.