The expressions of insulin-like growth factors, their receptors, and binding proteins are related to the mechanism regulating masseter muscle mass in the rat
The expressions of insulin-like growth factors, their receptors, and binding proteins are related to the mechanism regulating masseter muscle mass in the rat
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DOI：
10.1016/j.archoralbio.2006.01.003
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发表时间：
2006-07-01
影响因子：
3
通讯作者：
Yamane, A.
中科院分区：
文献类型：
--
作者：
Matsumoto, T.;Akutsu, S.;Yamane, A.
目的：骨骼肌质量调节机制尚不清楚。本研究的目的是研究胰岛素样生长因子（IGFs）、其受体（igfr）和结合蛋白（igfbp）在骨骼肌质量调节中的作用程度。设计：我们测量了口服克仑特罗3周后肥大的大鼠咬肌中IGFs、igfr和igfbp的mRNA表达水平，并确定咬肌重量与mRNA表达水平的相关性。结果：IGF-I、IGFR1、igfr2、IGFBP4、igfbp6 mRNA表达水平呈瘦肉精诱导的升高，且与咬肌重量呈正相关。IGFBP3仅表现出克仑特罗诱导的下降，且与咬肌重量呈负相关。IGFBP2和igfb5 mRNA表达量在对照组和盐酸克仑特罗组间无显著变化，且无显著相关性。IGFBP1 mRNA未检出。结论：上述结果提示IGF-I、II、IGFR1、2和IGFBP3、4、6与大鼠咬肌质量调节机制有关。(c) 2006 Elsevier Ltd.版权所有。
Objective: The mechanism regulating skeletal muscle mass is unclear. The purpose of the present study was to investigate the extent to which insutin-like growth factors (IGFs), their receptors (IGFRs), and binding proteins (IGFBPs) are involved in the regulation of skeletal muscle mass.Design: We measured the mRNA expression levels for IGFs, IGFRs, and IGFBPs in the rat masseter muscle hypertrophied by oral administration of clenbuterol for 3 weeks and determined the correlations between the weight of masseter muscle and the mRNA expression levels.Results: The mRNA expression levels for IGF-I and II, IGFR1 and 2, and IGFBP4 and 6 showed clenbuterol-induced elevations and positive correlations with the weight of masseter muscle. That for IGFBP3 only exhibited a clenbuterol-induced decrease and a strong negative correlation with the weight of masseter muscle. The mRNA expression levels for IGFBP2 and 5 showed no significant changes between the control and clenbuterol groups, and no significant correlations. IGFBP1 mRNA was not detectable.Conclusion: These results suggest that IGF-I, II, IGFR1 and 2, and IGFBP3, 4 and 6 are related to the mechanism regulating masseter muscle mass in the rat. (c) 2006 Elsevier Ltd. All rights reserved.