Osteoporosis as a Complication of Diabetes

Abstract

Bone fractures occur 5-7 times more often with type 1 diabetes, and type 2 diabetes was also recently identified as a risk factor for fractures (relative risk, 1.4-1.7). Moreover, poor blood glucose control results in a high prevalence of bone fracture in patients with type 2 diabetes. In addition to diabetic neuropathy, nephropathy, and retinopathy, arteriosclerotic diseases are also a common complication of diabetes. Therefore, osteoporosis should be considered as a complication or sequela of diabetes. Insulin secretion stimulates osteoblast maturation; in contrast, osteocalcin and sclerostin, which are involved in bone metabolism, affect insulin secretion and sensitivity. Furthermore, resting energy expenditure was associated with a serum bone turnover marker in postmenopausal women with type 2 diabetes in our cross-sectional study. An interplay between glucose metabolism and bone metabolism has been identified both in vitro and in vivo, and the pathology of osteoporosis differs between type 1 and type 2 diabetes. Although it is difficult to diagnose osteoporosis before a fracture, the early diagnosis of osteoporosis by considering glucose metabolism in patients with diabetes is important. In this review, the pathophysiology of osteoporosis in patients with diabetes and the effect of glucose metabolism are discussed.