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肥胖模型中下颌骨密度降低和成骨细胞胰岛素信号转导

Decreased jaw bone density and osteoblastic insulin signaling in a model of obesity.

机构信息

Department of Oral Biology and Diagnostic Science, Faculty of Dentistry.

出版信息

J Dent Res. 2013 Jun;92(6):560-5. doi: 10.1177/0022034513485600. Epub 2013 Apr 8.

DOI:10.1177/0022034513485600
PMID:23569161
Abstract

Previous studies have demonstrated that decreased bone mass results from either the impairment of osteoblastic insulin signaling or obesity. Our previous study revealed that 12-week high-fat-diet (HFD) consumption caused obesity as well as peripheral and brain insulin resistance. However, the osteoblastic insulin resistance induced by HFD has not been elucidated. Therefore, we hypothesized that 12-week HFD rats exhibited not only peripheral insulin resistance but also osteoblastic insulin resistance, which leads to decreased jawbone quality. We found that the jawbones of rats fed a 12-week HFD exhibited increased osteoporosis. The osteoblastic cells isolated from HFD-fed rats exhibited the impairment of osteoblastic insulin signaling as well as reduction of cell proliferation and survival. In conclusion, this study demonstrated that insulin resistance induced by 12-week HFD impaired osteoblastic insulin signaling, osteoblast proliferation, and osteoblast survival and resulted in osteoporosis in the jawbone.

摘要

先前的研究表明,骨量减少是由于成骨细胞胰岛素信号受损或肥胖所致。我们之前的研究表明,12 周高脂肪饮食(HFD)的摄入会导致肥胖以及外周和大脑胰岛素抵抗。然而,HFD 引起的成骨细胞胰岛素抵抗尚未阐明。因此,我们假设 12 周 HFD 大鼠不仅表现出外周胰岛素抵抗,而且表现出成骨细胞胰岛素抵抗,从而导致颌骨质量下降。我们发现,12 周 HFD 喂养的大鼠的颌骨表现出骨质疏松症增加。从 HFD 喂养的大鼠中分离出的成骨细胞表现出成骨细胞胰岛素信号受损,以及细胞增殖和存活减少。总之,这项研究表明,12 周 HFD 诱导的胰岛素抵抗会损害成骨细胞胰岛素信号、成骨细胞增殖和成骨细胞存活,从而导致颌骨骨质疏松症。

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