Multiple regression analyses adjusted for age, duration of diabetes, hemoglobin A1c, body mass index and log (serum creatinine) showed that serum UA level was significantly and negatively associated with uNTX in postmenopausal women with T2DM, whereas it was not associated with osteocalcin or BMD at each site.
The presence of FDR remained a predictor for decreased serum osteocalcin levels after adjusting for body mass index, blood glucose, blood lipids, and LFC (standardized β = - 0.057, P = 0.028).
Serum ucOC and OC concentrations remained significant factors even after adjusting for gender, HbA1c, body weight-adjusted total daily dose of insulin and duration of diabetes (β = -0.260, P = 0.027; β = -0.254, P = 0.031, respectively).
In late postmenopausal women, lower OC and CTX levels were associated with similarly increased risks of insulin resistance at baseline and incident diabetes over long-term follow-up.
With adjustment for age, irisin levels significantly correlated negatively with HbA1c% (r = -0.105, p < 0.001), years of diabetes (r = -0.07, p < 0.04), 25(OH)-Vitamin D (r = -0.175, p < 0.0001), and positively with BTT-Z-score (r = 0.088, p = 0.016), and osteocalcin (r = 0.059, p < 0.04).
The group with baseline osteocalcin levels <6.1 ng/mL showed a significantly higher risk for developing diabetes than the group with baseline osteocalcin levels >6.1 ng/mL (log-rank test, P < 0.0001) during the mean observation period (7.6 ± 6.1 years; mean ± SD).
Adult male Sprague Dawley (SD) rats were fed chow or high fat diet (HFD) for 8 weeks, and then diabetes was induced with an injection of low-dose streptozotocin (STZ) and treated daily with intraperitoneal injections of OCN for 12 weeks.
Although inversely correlated with serum glucose insulin and glycated haemoglobin, it is unclear whether OC reduction is caused by diabetes or plays a role in the pathogenesis and/or progression of the disease.
This review summarizes the molecular mechanisms involved in the modulation of OC expression, and discusses the potential relevance of OC in the pathogenesis and treatment of diabetes.
Our study was sufficiently powered to exclude BGLAP variants as a major risk factor (OR > 1.5) for T2D in Caucasians, but coding variants in exon 4 may alter glucose homeostasis and diabetes risk in African Americans.
Impaired bone formation due to defective osteoblast function, as reflected in a decreased serum osteocalcin (OC) concentration in the patients with diabetes, has been implicated in the development of diabetic osteopenia.