{"title":"[Bone fragility in type 1 diabetes and type 2 diabetes.]","authors":"Tomoyasu Fukui, Yasuyoshi Takahashi","doi":"CliCa19015156","DOIUrl":null,"url":null,"abstract":"<p><p>Diabetes mellitus causes hyperglycemia due to resistance to insulin action in peripheral organs in addition to progressive loss of β-cell function, thus it is involved in the development and progression of diabetic microangiopathy(retinopathy, nephropathy, and neuropathy). In addition, abnormalities of bone metabolism is regarded as a chronic complication related to both type 1 diabetes and type 2 diabetes. Accumulating evidence suggests that type 1 diabetes patients had decreased bone mineral density(BMD)and the fracture risk in the femoral neck is markedly higher, when compared to non-diabetic patients. A lack of insulin level in the portal vein is associated with systemic deficiencies of Insulin-like growth factor-1(IGF-1), known as growth-promoting polypeptide essential for promoting growth and bone formation. Thus, loss of IGF-1 play a crucial role for the pathogenesis of reduced BMD in type 1 diabetes. In type 2 diabetes, despite high bone mineral density with obesity, several studies have shown that men and women with type 2 diabetes mellitus are at increased risk for bone fracture. In other words, unlike type 1 diabetes patients, an increase in the risk of fracture in type 2 diabetes is significantly related to compromised bone quality, the other factor of impaired bone strength.</p>","PeriodicalId":10389,"journal":{"name":"Clinical calcium","volume":"29 1","pages":"51-56"},"PeriodicalIF":0.0000,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical calcium","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/CliCa19015156","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Diabetes mellitus causes hyperglycemia due to resistance to insulin action in peripheral organs in addition to progressive loss of β-cell function, thus it is involved in the development and progression of diabetic microangiopathy(retinopathy, nephropathy, and neuropathy). In addition, abnormalities of bone metabolism is regarded as a chronic complication related to both type 1 diabetes and type 2 diabetes. Accumulating evidence suggests that type 1 diabetes patients had decreased bone mineral density(BMD)and the fracture risk in the femoral neck is markedly higher, when compared to non-diabetic patients. A lack of insulin level in the portal vein is associated with systemic deficiencies of Insulin-like growth factor-1(IGF-1), known as growth-promoting polypeptide essential for promoting growth and bone formation. Thus, loss of IGF-1 play a crucial role for the pathogenesis of reduced BMD in type 1 diabetes. In type 2 diabetes, despite high bone mineral density with obesity, several studies have shown that men and women with type 2 diabetes mellitus are at increased risk for bone fracture. In other words, unlike type 1 diabetes patients, an increase in the risk of fracture in type 2 diabetes is significantly related to compromised bone quality, the other factor of impaired bone strength.