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ABSTRACT
The mechanism underlying diabetic osteopenia is still unclear and may involve obsteoblast activity and/or the deficit of insulin's anabolic action. One of the suggested etiopathogenetic mechanisms is decrement of osteoblastic functions and/or osteoblast number. Serum osteocalcin is a reliable marker of osteoblastic activity and of the bone formation index. In this study, we aimed to investigate the effect of diabetes on serum osteocalcin levels and to determine whether achieving the metabolic control by insulin therapy, further ameliorates these levels. Thirty four poorly controlled type II diabetic men (mean age; 43.7±4.6) were enrolled to the study. Mean duration of diabetes was 8.6 ±1.3 year, body mass index was < 27. Basal and 2nd, 4th, 8th weeks after insulin treatment serum PTH, osteocalcin, alkaline phosphatase, phosphorus, magnesium, HbA1c, 24 hour urine hydroxyproline levels were measured. in NIDDM patients serum osteocalcin levels were significantly lower when compared to the sex and age matched control group (12.9±2.6 ng/ml and 20.6±2.7 ng/ml respectively). No significant relationships were observed between osteocalcin levels, duration of diabetes and gfycosylated haemoglobin values. HbA1c levels decreased significantly after 8 weeks of insulin treatment, but in spite of the decrease in HbA1c, there were no significant changes in biochemical parameters of bone metabolism. In conclusion, after 8 weeks of insulin therapy and achieving good metabolic control, no amelioration in the osteocalcin levels were obtained. The observations suggest that osteoblast function and/or osteoblast number is not affected by insulin therapy or that an 8-week period of treatment not enough to change the biochemical parameters of bone formation.
The mechanism underlying diabetic osteopenia is still unclear and may involve obsteoblast activity and/or the deficit of insulin's anabolic action. One of the suggested etiopathogenetic mechanisms is decrement of osteoblastic functions and/or osteoblast number. Serum osteocalcin is a reliable marker of osteoblastic activity and of the bone formation index. In this study, we aimed to investigate the effect of diabetes on serum osteocalcin levels and to determine whether achieving the metabolic control by insulin therapy, further ameliorates these levels. Thirty four poorly controlled type II diabetic men (mean age; 43.7±4.6) were enrolled to the study. Mean duration of diabetes was 8.6 ±1.3 year, body mass index was < 27. Basal and 2nd, 4th, 8th weeks after insulin treatment serum PTH, osteocalcin, alkaline phosphatase, phosphorus, magnesium, HbA1c, 24 hour urine hydroxyproline levels were measured. in NIDDM patients serum osteocalcin levels were significantly lower when compared to the sex and age matched control group (12.9±2.6 ng/ml and 20.6±2.7 ng/ml respectively). No significant relationships were observed between osteocalcin levels, duration of diabetes and gfycosylated haemoglobin values. HbA1c levels decreased significantly after 8 weeks of insulin treatment, but in spite of the decrease in HbA1c, there were no significant changes in biochemical parameters of bone metabolism. In conclusion, after 8 weeks of insulin therapy and achieving good metabolic control, no amelioration in the osteocalcin levels were obtained. The observations suggest that osteoblast function and/or osteoblast number is not affected by insulin therapy or that an 8-week period of treatment not enough to change the biochemical parameters of bone formation.