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“Introduction Recently, Lee et al.  have described a novel function of the skeleton on energy metabolism. Specially, they demonstrated that the osteoblast-specific protein, osteocalcin, is involved in glucose
metabolism by increasing selleck products insulin secretion and cell proliferation in pancreatic β-cells and improving insulin sensitivity by upregulating the expression of an insulin-sensitizing adipokine (the adiponectin gene) in adipocytes. Subsequent human studies, including our own work, have confirmed the previous report [2–10]. Collectively, these human studies have shown that the serum osteocalcin concentration is negatively associated with the plasma glucose level and body check details fat mass [3, 5–7] and positively associated with insulin secretion [4, 8], lower insulin resistance [5–9], and serum
adiponectin concentration [3, 9]. In addition, Kanazawa et al.  showed that the serum osteocalcin level is negatively associated with the brachial-ankle SDHB pulse wave velocity and carotid intima-media thickness and suggested that osteocalcin might, thus, be linked to atherosclerosis. To date, homeostasis model assessment (HOMA) values have mainly been used to assess β-cell function and insulin sensitivity and the involvement of osteocalcin on glucose metabolism. However, the HOMA β-cell function index (HOMA-B%) is proportional to the fasting insulin level and is expected to be inversely related to insulin sensitivity in subjects with normal glucose tolerance (NGT), and thus, adjustment for insulin sensitivity is necessary . Also, the agreement between homeostasis model assessment insulin resistance (HOMA-IR), an indicator of insulin resistance, and clamp-measured insulin sensitivity is controversial, ranging from very good to nonexistent . Therefore, it is necessary to determine the association between osteocalcin and insulin secretion and insulin sensitivity with more valid methods. In addition, it remains uncertain whether or not the insulin-sensitizing and glucose-lowering effects of osteocalcin are truly mediated by upregulation of the adiponectin gene in humans.