期刊
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
卷 289, 期 5, 页码 E735-E745出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00159.2005
关键词
type 1 diabetes mellitus; type 2 diabetes mellitus; osteoblasts; osteoporosis; insulin receptors; hyperinsulinism
资金
- NCRR NIH HHS [C06 RR016517, C06 RR-16517] Funding Source: Medline
- NIDDK NIH HHS [R01 DK055653-01, R01 DK055653-07, R01 DK055653-04, DK-055653, R01 DK055653-05S1, R01 DK055653-02, R01 DK055653-08, R01 DK062999, R01 DK055653, R01 DK055653-05, R01 DK055653-03, R01 DK055653-06A2, DK-62999-04] Funding Source: Medline
Diabetic osteoporosis is increasingly recognized as a significant comorbidity of type 1 diabetes mellitus. In contrast, type 2 diabetes mellitus is more commonly associated with modest increases in bone mineral density for age. Despite this dichotomy, clinical, in vivo, and in vitro data uniformly support the concept that new bone formation as well as bone microarchitectural integrity are altered in the diabetic state, leading to an increased risk for fragility fracture and inadequate bone regeneration following injury. In this review, we examine the contribution that insulin, as a potential anabolic agent in bone, may make to the pathophysiology of diabetic bone disease. Specifically, we have assimilated human and animal data examining the effects of endogenous insulin production, exogenous insulin administration, insulin sensitivity, and insulin signaling on bone. In so doing, we present evidence that insulin, acting as an anabolic agent in bone, can preserve and increase bone density and bone strength, presumably through direct and/or indirect effects on bone formation.
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