Klein Gordon L
Gordon L Klein, Department of Orthopaedic Surgery and Rehabilitation, University of Texas and Shriners Burns Hospital, Galveston, TX 77555, United States.
World J Diabetes. 2014 Feb 15;5(1):14-6. doi: 10.4239/wjd.v5.i1.14.
While insulin-like growth factor I is a well-known anabolic agent in bone evidence is beginning to accumulate that its homologue, insulin, also has some anabolic properties for bone. There is specific evidence that insulin may work to stimulate osteoblast differentiation, which in turn would enhance production of osteocalcin, the osteoblast-produced peptide that can stimulate pancreatic β cell proliferation and skeletal muscle insulin sensitivity. It is uncertain whether insulin stimulates bone directly or indirectly by increasing muscle work and therefore skeletal loading. We raise the question of the sequence of events that occurs with insulin resistance, such as type 2 diabetes. Evidence to date suggests that these patients have lower serum concentrations of osteocalcin, perhaps reduced skeletal loading, and reduced bone strength as evidenced by micro-indentation studies.
虽然胰岛素样生长因子-I是一种众所周知的骨骼合成代谢因子,但越来越多的证据表明,其同系物胰岛素对骨骼也具有一些合成代谢特性。有具体证据表明,胰岛素可能通过刺激成骨细胞分化发挥作用,而成骨细胞分化反过来又会增强骨钙素的生成,骨钙素是一种由成骨细胞产生的肽,能够刺激胰腺β细胞增殖和骨骼肌胰岛素敏感性。目前尚不清楚胰岛素是直接刺激骨骼,还是通过增加肌肉活动从而增加骨骼负荷来间接刺激骨骼。我们提出了胰岛素抵抗(如2型糖尿病)时所发生事件顺序的问题。迄今为止的证据表明,这些患者血清骨钙素浓度较低,可能存在骨骼负荷降低,并且微压痕研究证明其骨强度降低。