title: Impaired secretion of parathyroid hormone, but not refractoriness of osteoblast, is a major mechanism of low bone turnover in hemodialyzed patients with diabetes mellitus.
abstract: Diabetic bone disease is characterized by low bone turnover resulting from either impaired secretion of parathyroid hormone (PTH) or refractoriness of osteoblasts to PTH. The present study was performed to elucidate which factor contributes more to the reduction in bone turnover by comparison between 64 hemodialyzed patients with diabetes mellitus and 106 hemodialyzed patients without diabetes mellitus. Only men were enrolled to avoid the influence of the menstrual cycle on bone metabolism. Serum intact PTH (iPTH) levels were significantly lower in hemodialyzed patients with diabetes than those without diabetes, although no significant difference existed in age, duration of hemodialysis therapy, or serum calcium or phosphate levels. Of the biochemical markers measured, serum intact osteocalcin (iOC) and deoxypyridinoline levels were significantly lower in patients with diabetes, although serum bone-specific alkaline phosphatase (BAP) and pyridinoline levels did not differ significantly between the two groups of patients. When patients were restricted to those with serum iPTH levels greater than 180 pg/mL, this parameter correlated significantly in a positive manner with both serum iOC and BAP levels and negatively with bone mineral density at distal radius 1/3. Regression slopes between iPTH levels and these parameters were not significantly different between the two groups of patients, indicating the absence of refractoriness of bone to PTH in patients with diabetes. In conclusion, our findings suggest that impaired PTH secretion, but not refractoriness of osteoblasts to PTH, may be responsible for the low bone turnover in hemodialyzed patients with diabetes.
authors.affiliation: Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan. inaba-m@med.osaka-cu.ac.jp
authors.forename: Masaaki
authors.initials: M
authors.lastname: Inaba
authors.forename: Kyoko
authors.initials: K
authors.lastname: Nagasue
authors.forename: Senji
authors.initials: S
authors.lastname: Okuno
authors.forename: Misako
authors.initials: M
authors.lastname: Ueda
authors.forename: Yasuro
authors.initials: Y
authors.lastname: Kumeda
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Imanishi
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Shoji
authors.forename: Eiji
authors.initials: E
authors.lastname: Ishimura
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Ohta
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Nakatani
authors.forename: Masao
authors.initials: M
authors.lastname: Kim
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Nishizawa
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D015519:Bone Density; D001842:Bone and Bones / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000378:metabolism* / Q000628:therapy*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism / Q000628:therapy; D008159:Lumbar Vertebrae / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010006:Osteoblasts / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000097:blood / Q000378:metabolism*; D011884:Radius / Q000378:metabolism; D006435:Renal Dialysis
chemical_list: D015415:Biomarkers; D010281:Parathyroid Hormone