4.7 Article

Adiponectin Is Associated with Changes in Bone Markers during Glycemic Control in Type 2 Diabetes Mellitus

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JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
卷 94, 期 8, 页码 3031-3037

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ENDOCRINE SOC
DOI: 10.1210/jc.2008-2187

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  1. Japan Osteoporosis Society

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Objective: Although several experiments show that adiponectin is associated with bone metabolism, a relationship between adiponectin and bone markers is still unclear. We monitored chronological changes in hyperglycemia, serum adiponectin, and bone markers during glycemic control in type 2 diabetes and analyzed relationships among these parameters. Subjects and Results: A total of 50 Japanese patients with poorly controlled type 2 diabetes [initial hemoglobin A(1c) (HbA(1c)) = 10.0 +/- 2.5%] were recruited, and biochemical data were collected before and after glycemic control for a month. Of bone formation markers, bone-specific alkaline phosphatase was decreased with a mean change of -3.11 [95% confidence interval (CI), -5.03 to -1.20; P < 0.01], whereas osteocalcin (OC) was increased with a mean change of 1.94 (95% CI, 1.45-2.42; P < 0.001) and undercarboxylated OC (ucOC)/OC ratio was decreased with a mean change of -0.15 (95% CI, -0.27 to -0.03; P < 0.01). Although adiponectin level was not significantly different before and after glycemic control, baseline adiponectin level, but not HbA1c, was positively correlated with changes in OC, ucOC, and urinary N-terminal cross-linked telopeptide of type I collagen (uNTX) (r = 0.30, P = 0.04; r = 0.32, P = 0.03; and r = 0.36, P = 0.01, respectively). Changes in adiponectin were also negatively correlated with changes in OC and uNTX (r = -0.42, P < 0.01; and r = -0.38, P < 0.01, respectively). Changes in HbA(1c) were negatively correlated with changes in OC (r = -0.30, P = 0.03). Conclusion: These findings show that treatments for hyperglycemia enhance OC level and suggest that serum adiponectin level before starting to compensate poorly controlled diabetics could predict the subsequent improvement of bone remodeling markers during glycemic control. (J Clin Endocrinol Metab 94: 3031-3037, 2009)

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