骨重建
成骨细胞
内分泌学
胰岛素受体
胰岛素
内科学
破骨细胞
骨吸收
PI3K/AKT/mTOR通路
信号转导
胰岛素抵抗
蛋白激酶B
生物
细胞生物学
化学
医学
受体
生物化学
体外
作者
Sakarat Pramojanee,Mattabhorn Phimphilai,Nipon Chattipakorn,Siriporn C. Chattipakorn
标识
DOI:10.3109/07435800.2013.879168
摘要
Insulin and its downstream signaling pathway are indispensable for postnatal bone growth and turnover by having influence on both osteoblast and osteoclast development. Insulin signaling regulates both bone formation by osteoblasts and bone resorption by osteoclasts; however, the regulation occurs mainly through the insulin signaling pathway within osteoblasts. An impairment of osteoblastic insulin signaling leads to an impaired bone quality by affecting osteoblast proliferation, differentiation and survival. The insulin signaling pathway and MAPK and PI3K/Akt pathways play pivotal roles in the differentiation, function and survival of bone cells. Current evidence suggests that osteoblastic insulin signaling not only modulates bone growth and turnover but is also required for energy metabolism. Several mice models with impaired insulin signaling exhibited both bone and metabolic phenotypes, including symptoms of low bone mass, obesity, glucose intolerance and insulin resistance. In this review, we discuss the key findings that suggest a pivotal role of osteoblastic insulin signaling in both bone and energy metabolism.
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