Bone Regulates Glucose Metabolism as an Endocrine Organ through Osteocalcin

<div>Proposed regulation of<i> Esp</i> expression and OCN carboxylation in mice. FoxO1 and ATF4 could bind to the promoter site to stimulate the transcription of<i> Esp</i>. The product of<i> Esp</i> is OST-PTP, which can suppress the carboxylation of prepro-OCN and in turn suppress the activity of OCN. V<sub>K</sub>, Vitamin K; SNS, sympathetic nervous system; OCN, osteocalcin; ucOCN, uncarboxylated osteocalcin.</div>

International Journal of Endocrinology

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Figure 4

Figure 4: Bone Regulates Glucose Metabolism as an Endocrine Organ through Osteocalcin 