Few reports are available on bone turnover in type 2 diabetes. Impaired bone turnover in type 2 diabetes appears to result from decreased bone formation. Studies also suggest that poor glycaemic control in type 2 diabetes may contribute to osteopaenia. The aim of this study was to investigate biochemical markers of bone turnover in males with poorly controlled type 2 diabetes and look for correlations with glycaemic control and gonadal and hypophyseal hormonal axis. Consecutive male patients with poorly controlled type 2 diabetes and attending the internal medicine department during a period of 6 months were enrolled. The patients were receiving oral hypoglycaemic agents (metformin or sulphonylureas or both). None of the patients had any evidence of macroangiopathy, nephropathy or neuropathy. Only two patients had proliferative retinopathy. Serum osteocalcin, crosslaps (C-telopeptide, CTx), parathyroid hormone (PTH), testosterone, oestrogen, prolactin, follicle-stimulating hormone (FSH) and luteinising hormone (LH) were measured in 35 patients and 35 controls. The mean age of the study population was 53.7 (10.3) years (range: 50.2-57.3) and the mean disease duration was 8.6 (6.0) years (range: 6.5-10.7). No differences between patients and controls were observed in serum calcium, phosphorus, creatinine, albumin, PTH, CTx, oestrogen, testosterone, LH, FSH, prolactin and urinary calcium. Patients had lower serum levels of osteocalcin than controls with a significant statistical difference [15.3 (4.1) vs 18.3 (5.3), p=0.012]. There was a negative significant statistical correlation between CTx levels and HbA1c (r=-0.41, p< 0.05). Our study suggested that bone formation is altered in type 2 diabetes and that bone turnover is affected by glycaemic control status.

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