Secondary osteoporosis and its treatment--diabetes mellitus

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.