Elucidation of involved mechanisms impaired for insulin secretion due to oxidative stress and macrophages in pancreatic islets of type 2 diabetes.
阐明 2 型糖尿病胰岛中氧化应激和巨噬细胞导致胰岛素分泌受损的相关机制。
基本信息
- 批准号:19591065
- 负责人:
- 金额:$ 2.83万
- 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:2007
- 资助国家:日本
- 起止时间:2007 至 2009
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
The increased release of MCP-1 was observed from pancreatic MIN6 β cells under diabetic conditions, leading to the enhancement of macrophage infiltration into pancreatic islets. And increased endogenous oxidative stress in β cells could be related to its underlying mechanism. In addition, the release of MCP-1 and VEGF was also found to be increased from 3T3L1 adipocytes. The enhancement of endogenous oxidative stress was similarly speculated to be the pathogenic mechanism of their increased secretion, and in terms of released MCP-1, we deduce that the IkB- dependent pathway is, at lease in part, important as a common distal signaling in both pancreatic β cells and adipocytes.
在糖尿病条件下观察到胰腺 MIN6 β 细胞释放 MCP-1 增加,导致巨噬细胞浸润胰岛的增强,并且 β 细胞内源性氧化应激的增加可能与其释放的机制有关。还发现 3T3L1 脂肪细胞的 MCP-1 和 VEGF 增加。同样推测内源性氧化应激的增强是其致病机制。分泌增加,并且就释放的 MCP-1 而言,我们推断 IkB 依赖性途径作为胰腺 β 细胞和脂肪细胞中的常见远端信号传导至少在一定程度上是重要的。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Glucolipotoxicityによる膵β細胞からのMCP-1分泌の増加と細胞内情報伝達系の関与
由于糖脂毒性和细胞内信号转导系统的参与,胰腺 β 细胞的 MCP-1 分泌增加
- DOI:
- 发表时间:2008
- 期刊:
- 影响因子:0
- 作者:関博之;高橋和人;三代川可織;半田桂子;勝田秀紀;下山達宏;田中利明;山口真哉;吉元勝彦;板垣英二;永松信哉;石田均
- 通讯作者:石田均
膵β細胞からのMCP-1分泌に及ぼす高濃度グルコースおよび脂肪酸の影響について.
高浓度葡萄糖和脂肪酸对胰腺β细胞分泌MCP-1的影响。
- DOI:
- 发表时间:2007
- 期刊:
- 影响因子:0
- 作者:関 博之;石田 均;ら
- 通讯作者:ら
Hypoxia- independent VEGF120 secretion is stimulated by increase of endogenous oxidative stress through PI3K-dependent pathways in artificially hypertrophied 3T3-L1 adipocytes: The regulation by distinct mechanism from MCP-1 via JNK and p38 MAPK pathways
在人工肥大的 3T3-L1 脂肪细胞中,通过 PI3K 依赖性途径增加内源性氧化应激,刺激缺氧独立的 VEGF120 分泌:通过 JNK 和 p38 MAPK 途径通过与 MCP-1 不同的机制进行调节
- DOI:
- 发表时间:2010
- 期刊:
- 影响因子:0
- 作者:K. Takahashi;S. Yamaguchi;T. Shimoyama;T. Tanaka;K. Miyokawa;K. Handa;H. Katsuta;S. Nishida;K. Yoshimoto;H. Ishida
- 通讯作者:H. Ishida
肥大化脂肪細胞におけるVEGF120分泌の制御機構について-MCP-1分泌機構との相違-
关于肥大脂肪细胞中VEGF120分泌的控制机制 - 与MCP-1分泌机制的差异 -
- DOI:
- 发表时间:2009
- 期刊:
- 影响因子:0
- 作者:高橋和人;山口真哉;下山達宏;田中利明;三代川可織;半田桂子;勝田秀紀;西田進;吉元勝彦;永松信哉;石田均
- 通讯作者:石田均
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{{ truncateString('ISHIDA Hitoshi', 18)}}的其他基金
A study of the effects of discourses on Gay magazines to gay movements
同性恋杂志话语对同性恋运动影响的研究
- 批准号:
26883009 - 财政年份:2014
- 资助金额:
$ 2.83万 - 项目类别:
Grant-in-Aid for Research Activity Start-up
Elucidation of involved mechanisms for macrophage infiltration into pancreatic islets and of its role on the occurrence of type 2 diabetes.
阐明巨噬细胞浸润胰岛的相关机制及其在 2 型糖尿病发生中的作用。
- 批准号:
22590993 - 财政年份:2010
- 资助金额:
$ 2.83万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Molecular Design of Photocatalysts Based on 'Peptide Origami' toward Nitrite Reductase Mimics
基于“肽折纸”的亚硝酸还原酶模拟物光催化剂分子设计
- 批准号:
21550163 - 财政年份:2009
- 资助金额:
$ 2.83万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
New strategy for treatment of type 2 diabetes by utilizing the regeneration of pancreatic β cell function
利用胰腺β细胞功能再生治疗2型糖尿病的新策略
- 批准号:
15590955 - 财政年份:2003
- 资助金额:
$ 2.83万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Molecular Design of Artificial Proteins Bearing Novel Structural Motif by Utilizing an Unnatural Amino Acid
利用非天然氨基酸进行具有新颖结构基序的人工蛋白质的分子设计
- 批准号:
14380292 - 财政年份:2002
- 资助金额:
$ 2.83万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Molecular physiological and biological studies on the effect of free fatty acids on pancreatic β cell function
游离脂肪酸对胰腺β细胞功能影响的分子生理学和生物学研究
- 批准号:
12671126 - 财政年份:2000
- 资助金额:
$ 2.83万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Molecular physiological and biological studies on the mechanismof impaired glucose-induced insulin secretion in diabetes mellitus
糖尿病葡萄糖诱导胰岛素分泌受损机制的分子生理学和生物学研究
- 批准号:
09671048 - 财政年份:1997
- 资助金额:
$ 2.83万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Physiological and molecular biological studies on the pathogenesis of impaired insulin secretion in diabetes mellitus.
糖尿病胰岛素分泌受损发病机制的生理和分子生物学研究。
- 批准号:
07671128 - 财政年份:1995
- 资助金额:
$ 2.83万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Physiological and molecular biological studies on functional alterations in ion channels of pancreatic beta cells in diabetes mellitus.
糖尿病胰腺β细胞离子通道功能改变的生理和分子生物学研究。
- 批准号:
05670857 - 财政年份:1993
- 资助金额:
$ 2.83万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
Physiological and molecular biological studies on altered function of the intracellular signal transduction system in pancreatic beta cells of diabetes mellitus.
糖尿病胰腺β细胞细胞内信号转导系统功能改变的生理和分子生物学研究。
- 批准号:
03671145 - 财政年份:1991
- 资助金额:
$ 2.83万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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Mechanistic study on defects in pancreatic beta-cell function, and its prevention by food factors
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建立“还原应激”的组学分析,这是一种由过度抗氧化和还原环境引起的生物紊乱
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糖尿病条件下改善胰腺β细胞功能的目标因素的鉴定和分析
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Function-structure relationship; role of the islet Schwann cells
功能结构关系;
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