Kumeda Y, Inaba M, Nishizawa Y
Second Department of Internal Medicine, Osaka City University Medical School.
Nihon Rinsho. 1998 Jun;56(6):1579-86.
Japanese epidemiological study showed higher frequency of osteopenia/osteoporosis in diabetic patients as compared with sex- and age-matched control. The mechanism by which bone loss occurs in diabetic patients could be explained by a reduction of insulin/insulin-like growth factor-I action, sustained hyperglycemic state, a generation of advanced glycosylation end-products, and diabetic complication such as neuropathy, nephropathy and myopathy. Osteoblast deficit is hypothesized to play a major role in the occurrence of diabetic osteopenia. Besides the deficiency of insulin and insulin-like growth factor-I, we demonstrated that sustained hyperglycemia alone causes suppression of osteoblast proliferation and its response to parathyroid hormone and 1 alpha, 25-dihydroxyvitamin D, Hyporesponse of osteoblast to 1 alpha, 25-dihydroxyvitamin D, was also confirmed in diabetic patients as reflected by a reduction in an incremental response of serum osteocalcin during 1 alpha, 25-dihydroxyvitamin D administration. The regimens having stimulatory effect on bone turnover, such as intermittent PTH therapy and vitamin D, are recommended to treat diabetic osteopenia, besides improvement of diabetic control state.
日本的一项流行病学研究表明，与年龄和性别匹配的对照组相比，糖尿病患者中骨质减少/骨质疏松的发生率更高。糖尿病患者发生骨质流失的机制可以通过胰岛素/胰岛素样生长因子-I作用的降低、持续的高血糖状态、晚期糖基化终产物的产生以及糖尿病并发症（如神经病变、肾病和肌病）来解释。据推测，成骨细胞缺陷在糖尿病性骨质减少的发生中起主要作用。除了胰岛素和胰岛素样生长因子-I缺乏外，我们还证明，单纯持续高血糖会导致成骨细胞增殖受抑制及其对甲状旁腺激素和1α,25-二羟维生素D的反应受抑制。糖尿病患者中，成骨细胞对1α,25-二羟维生素D反应低下也得到了证实，这表现为在给予1α,25-二羟维生素D期间血清骨钙素的增量反应降低。除了改善糖尿病控制状态外，建议采用对骨转换有刺激作用的治疗方案，如间歇性甲状旁腺激素治疗和维生素D治疗，来治疗糖尿病性骨质减少。
