Roles of autonomic nervous system in inter-organ metabolic communication.

自主神经系统在器官间代谢通讯中的作用。

• 批准号: 21790859
• 负责人: YAMADA Tetsuya
• 金额: $ 2.75万
• 依托单位: Tohoku University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21790859/
• 关键词: 肥満; 糖尿病; エネルギー代謝; 自律神経; 肥満症; 自律神経系; 視床下部; 肝臓; 求心性神経経路; 臓器間相互作用

The incidence of obesity is rising at epidemic proportions. Several mechanisms underlying the normalization of body weight following involuntary overfeeding are demonstrated ; however, the same excess amount of energy intake resulting from overfeeding does not evoke the same degree of body weight gain. We identified a novel inter-organ communication via neuronal pathway, which suppresses energy expenditure in over-nutritious state. By studying a mouse model, we found out that hepatic glucokinase expression precedes body weight gain due to high fat feeding, and showed that adenovirus-mediated expression of glucokinase in the liver suppressed energy expenditure, resulting in body weight gain. These responses are mediated by a neuronal pathway linking liver, afferent vagus, raphe palllidus, efferent sympathetic nerve, and finally brown adipose tissue, in this order. Furthermore, leptin-induced energy expenditure, primarily observed in overnutritious state, was suppressed by this pathway.

肥胖症的发生率在流行比例时升高。证明了非自愿过度喂养后体重归一化的几种机制；但是，过量喂养引起的相同大量的能量摄入不会引起体重增加的程度。我们通过神经元途径确定了一种新型的器官间通信，该通道抑制了过度努力状态的能量消耗。通过研究小鼠模型，我们发现肝葡萄糖激酶表达在高脂肪进食引起的体重增加之前，并表明腺病毒介导的葡萄糖酶在肝脏抑制能量消耗中的表达，导致体重增加。这些反应是由连接肝脏，传入的迷走神经，raphe palllidus，传出的交感神经，最后是棕色脂肪组织的神经元途径介导的。此外，该途径抑制了瘦素诱导的能量消耗，主要在营养状态下观察到。

项目成果

Characterization of a novel murine preadipocyte line, AP-18, isolated from subcutaneous tissue : analysis of adipocyte-related gene expressions

从皮下组织分离的新型小鼠前脂肪细胞系 AP-18 的表征：脂肪细胞相关基因表达的分析

• 发表时间: 2010
• 期刊: Cell Biol Int. 34(3)
• 作者: Chen C;Takahashi K;Yoshida A;Takizawa Y;Lee Y;Nakui M;Doi H;Takebayashi Y;Fukumoto M;Yamada T;Katagiri H;Oka Y;Satoh J.
• 通讯作者: Satoh J.

Interleukin-6 Enhances Glucose-Stimulated Insulin Secretion From Pancreatic β-Cells : Potential Involvement of the PLC-IP3-Dependent Pathway.

Interleukin-6 增强胰腺 β 细胞葡萄糖刺激的胰岛素分泌：PLC-IP3 依赖性途径的潜在参与。

• 发表时间: 2011
• 期刊: Diabetes
• 影响因子: 7.7
• 作者: Suzuki T;Imai J;Yamada T;Ishigaki Y;Kaneko K;Uno K;Hasegawa Y;Ishihara H;Oka Y;Katagiri H.
• 通讯作者: Katagiri H.

神経系による代謝臓器連関

通过神经系统连接代谢器官

• 发表时间: 2011
• 期刊: メディカル・サイエンス・ダイジェスト
• 作者: 山田哲也;片桐秀樹
• 通讯作者: 片桐秀樹

メタボリックシンドロームと自律神経系

代谢综合征和自主神经系统

• 发表时间: 2009
• 期刊: Clinical Neuroscience 27(12)
• 作者: 山田哲也;片桐秀樹
• 通讯作者: 片桐秀樹

Characterization of a novel murine preadipocyte line, AP-18, isolated from subcutaneous tissue : analysis of adipocyte-related gene expressions.

从皮下组织分离的新型小鼠前脂肪细胞系 AP-18 的表征：脂肪细胞相关基因表达的分析。

• 发表时间: 2010
• 期刊: Cell Biol Int. 34(3)
• 作者: Chen C;Takahashi K;Yoshida A;Takizawa Y;Lee Y;Nakui M;Doi H;Takebayashi Y;Fukumoto M;Yamada T T;Katagiri H;Oka Y;Satoh J.
• 通讯作者: Satoh J.