A muscle secreting protein attractin regulates expression of UCP-2 in adipocytes.
肌肉分泌蛋白吸引素调节脂肪细胞中 UCP-2 的表达。
基本信息
- 批准号:16590175
- 负责人:
- 金额:$ 2.3万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2004
- 资助国家:日本
- 起止时间:2004 至 2005
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Prolonged spaceflight and bed-resting cause remark appetite loss. A lot of investigators suggest that this appetite loss is probably due to psychological stress. In the present study, we reasoned that skeletal muscle atrophied by unloading regulated energy consumption via a novel muscle-secreting enzyme, attractin. Our DNA microarray analysis revealed that skeletal muscle atrophied by unloading remarkably expressed the secreted-type attractin. In addition, starvation stimulated expression of attractin in skeletal muscle, indicating that energy intake may regulate attractin expression in the muscle. Our co-culturing system with 3T3-L1 adipocytes and attractin-overexpressing Cos7 cells showed that the secreted attractin from Cos7 cells stimulated expression of uncoupled protein-2 (UCP-2) in the adipocytes. This finding suggests that attractin may stimulate heat conversion in adipocytes and prevent the obesity. Up to now, there is no report about the factors regulating attractin expression. We found that only insulin decreased expression of attractin in skeletal muscle, indicating that blood glucose levels may be involved in attractin expression. Based on these findings, we propose that skeletal muscle may secrete several cytokines (so called myokines), and these myokines may regulate the growth and function of adipose tissues.
长时间的太空飞行和卧床休息会引起食欲减退。许多研究人员认为,这种食欲下降可能是由于心理压力。在本研究中,我们推断骨骼肌萎缩是通过一种新的肌肉分泌酶--吸引素--卸载调节的能量消耗。我们的DNA微阵列分析显示,因卸载而萎缩的骨骼肌显着表达分泌型吸引素。此外,饥饿刺激骨骼肌中吸引素的表达,表明能量摄入可以调节肌肉中吸引素的表达。我们用3 T3-L1脂肪细胞和过表达吸引素的Cos 7细胞共培养系统表明,Cos 7细胞分泌的吸引素刺激脂肪细胞中解偶联蛋白-2(UCP-2)的表达。这一发现表明,吸引素可以刺激脂肪细胞的热转换,防止肥胖。到目前为止,还没有关于吸引素表达调控因子的报道。我们发现,只有胰岛素降低骨骼肌中吸引素的表达,表明血糖水平可能参与吸引素的表达。基于这些发现,我们提出骨骼肌可能分泌几种细胞因子(所谓的肌因子),这些肌因子可能调节脂肪组织的生长和功能。
项目成果
期刊论文数量(42)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Osteoactivin upregulates expression of MMP-3 and MMP-9 in fibroblasts infiltrated into denervated skeletal muscle in mice
- DOI:10.1152/ajpcell.00565.2004
- 发表时间:2005-09-01
- 期刊:
- 影响因子:5.5
- 作者:Ogawa, T;Nikawa, T;Yasui, N
- 通讯作者:Yasui, N
Skeletal muscle gene expression in healthy volunteers with a 20-day-bed-rest.
卧床休息 20 天的健康志愿者的骨骼肌基因表达。
- DOI:
- 发表时间:2005
- 期刊:
- 影响因子:0
- 作者:Hirasaka K. et al.;Hirasaka K.et al.;Ogawa T.et al.;Ogawa T.et al.
- 通讯作者:Ogawa T.et al.
Clinorotation prevents differentiation of rat myoblastic cells in association with reduced NF-κB-Signaling.
旋转可防止与 NF-κB 信号传导减弱相关的大鼠成肌细胞分化。
- DOI:
- 发表时间:2005
- 期刊:
- 影响因子:0
- 作者:Hirasaka K. et al.
- 通讯作者:Hirasaka K. et al.
Osteoactivin up-regulates expression of MMPs-3 and 9 in fibroblasts infiltrated into denervated skeletal muscle in mice.
骨激活素上调小鼠去神经骨骼肌中浸润的成纤维细胞中 MMP-3 和 9 的表达。
- DOI:
- 发表时间:2005
- 期刊:
- 影响因子:0
- 作者:Hirasaka K. et al.;Hirasaka K.et al.;Ogawa T.et al.
- 通讯作者:Ogawa T.et al.
The role of ubiquitin ligase Cb1-b in denervation-mediated osteopenia.
泛素连接酶 Cb1-b 在去神经介导的骨质减少中的作用。
- DOI:
- 发表时间:2006
- 期刊:
- 影响因子:0
- 作者:Yamada A;et al.;中村晃(分担執筆);Suzue N. et al.
- 通讯作者:Suzue N. et al.
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KISHI Kyoichi其他文献
KISHI Kyoichi的其他文献
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{{ truncateString('KISHI Kyoichi', 18)}}的其他基金
Development of novel nutritional methods to inhibit muscle atrophy caused by microgravity.
开发新的营养方法来抑制微重力引起的肌肉萎缩。
- 批准号:
13660126 - 财政年份:2001
- 资助金额:
$ 2.3万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Abmormal expression of mitochondrial gene in disuse-induced muscle atrophy
废用性肌肉萎缩中线粒体基因的异常表达
- 批准号:
11670071 - 财政年份:1999
- 资助金额:
$ 2.3万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Protein intake regulation by the liver
肝脏对蛋白质摄入的调节
- 批准号:
60480121 - 财政年份:1985
- 资助金额:
$ 2.3万 - 项目类别:
Grant-in-Aid for General Scientific Research (B)