Relationships between serum osteocalcin levels versus blood glucose, insulin resistance and markers of systemic inflammation in central Indian type 2 diabetic patients.
نویسندگان
چکیده
BACKGROUND Recent studies have demonstrated an endocrine role of osteoblast derived protein osteocalcin in the regulation of blood glucose homeostasis. In addition emerging evidence suggests that subclinical inflammation is associated with altered bone metabolism. However, the relationship between osteocalcin and inflammatory markers is still unclear. AIM This study was aimed to investigate the association of serum osteocalcin with fasting plasma glucose, insulin resistance and markers of systemic inflammation - interleukin-6 (IL-6) and high sensitivity C-reactive protein (hs-CRP) in central Indian type 2 diabetic patients. PATIENTS AND METHODS This study included 108 individuals with newly diagnosed type 2 diabetes mellitus (DM) and 50 age and body mass index (BMI) matched healthy subjects as controls. Blood samples were analyzed for fasting plasma glucose, fasting insulin, interleukin-6, hs-CRP and serum osteocalcin. Insulin resistance was calculated by homeostasis model assessment (HOMA-IR). RESULTS In the present study we observed significantly lower level of osteocalcin in type 2 diabetic group compared to non diabetic control (p < 0.0001). In linear regression analysis adjusted for age, gender, BMI, waist circumference and waist to hip ratio, serum level of osteocalcin was inversely associated with fasting plasma glucose (beta = -0.015; p = 0.0004), fasting insulin (beta = -0.059; p = 0.0242), HOMA-IR (beta = -0.149; p = 0.0011), interleukin-6 (beta = -0.071; p = 0.0036) and hs-CRP levels (beta = -0.506; p = 0.0085) in the diabetic subjects. CONCLUSIONS Our findings suggest that osteoblast derived protein osteocalcin may have a wide ranging role in the pathophysiology of type 2 diabetes by being associated with both blood glucose homeostasis and systemic inflammation.
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عنوان ژورنال:
- European review for medical and pharmacological sciences
دوره 17 12 شماره
صفحات -
تاریخ انتشار 2013