title: Bone metabolism in male patients with type 2 diabetes.
abstract: 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.
authors.affiliation: Rheumatology and Physical Rehabilitation Department, Military Hospital Mohammed V, Rabat, Morocco.
authors.forename: Lahsen
authors.initials: L
authors.lastname: Achemlal
authors.forename: Saida
authors.initials: S
authors.lastname: Tellal
authors.forename: Fouad
authors.initials: F
authors.lastname: Rkiouak
authors.forename: Abderrazak
authors.initials: A
authors.lastname: Nouijai
authors.forename: Ahmed
authors.initials: A
authors.lastname: Bezza
authors.forename: El Mostapha
authors.initials: el M
authors.lastname: Derouiche
authors.forename: Driss
authors.initials: D
authors.lastname: Ghafir
authors.forename: Abdellah
authors.initials: A
authors.lastname: El Maghraoui
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D001862:Bone Resorption; D001842:Bone and Bones / Q000378:metabolism*; D003094:Collagen / Q000097:blood; D024042:Collagen Type I; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D006441:Hemoglobin A / Q000378:metabolism; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010012:Osteogenesis; D010455:Peptides / Q000097:blood; D013223:Statistics as Topic
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D024042:Collagen Type I; D007004:Hypoglycemic Agents; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; D015675:Osteocalcin; D003094:Collagen; D006441:Hemoglobin A