Signal transduction of dietary fat and energy metabolismsthrough nucrea receptor

通过核受体进行膳食脂肪和能量代谢的信号转导

• 批准号: 13460058
• 负责人: KAWADA Teruo
• 金额: $ 9.66万
• 依托单位: Kyoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2001
• 资助国家: 日本
• 起止时间: 2001 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-13460058/
• 关键词: OBESITY; LIPID METABOLISM; ENERGY METABOLISM; FAT; NUCREAR RECEPTOR; PPAR; AGONIST; ANTAGONIST

Obesity became the basis, namely principal factor of many generally known life, habit illness emergences, being related with sick condition emergence deeply was ascertained. As for this research, foundation of that kind of obesity formation it is not we pay attention to lipid metabolism and the energy exchangemechanism. The mechanism decisively carry out important role in hyperplasia of adipose tissue, relation between the control of revelation of knitting machine structure and differentiation formation of white and the brown fat cell was analyzed. As for the execution. people, so far, the long-chain fatty acid became the ligand in hyperplasia of obesity namely white adipose tissue and PPAR controlled gene revelation at transcriptional level as a master regulator, beginning discovered the fact that the function receives decoration furthermore with the various nutrients promptly in the world.At the time of this researching PPAR as a fatty acid sensor, lipid metabolism and energy metabol … More ism relating gene revelation are controlled with some kind of signal transduction mechanism whether the above-mentioned signal transduction mechanism, it receives the decoration with meal factor whether the lipid metabolism which decreases as for functional playback of energy exchange system possibility research. We analyzed clear 3 points as study purposes.As a result, PPAR controlling transcription of the.,lipid' metabolism and the energy exchange type gene having a meal the fatty acid of origin a ligand, furthermore in signal transduction system inside 'this cell coactivator factor of nuclear transcriptional factor, the especially CREB connection protein (CBP) with the PPAR ligand over saturation under condition, the revelation quantity Of the metabolism details electron being stipulated by the revelation quantity of CBP became clearr in vivo such as thing and the high fat food intake where that homolog p300 has participated deeply. In addition, it existed in brown adipose tissue and the deviation from coactivator protein which relates to body thermal production deeply (UCP) as for revelation the lipid metabolism which decreases from thefact that. it is controlled by PPAR, with PPAR ligand such as highly' unsaturated fatty acid and plant origin isoprenoid, possibility of functional playback of energy exchange system was suggested. Less

肥胖成为许多众所周知的生活、习惯性疾病发生的基础，即主要因素，与病情的发生有着深刻的关系。就本研究而言，那种肥胖形成的基础不是我们关注的脂质代谢和能量交换机制。在脂肪组织增生中起决定性作用的机制，分析了织机结构的显示控制与白色和棕色脂肪细胞分化形成的关系。至于处决。到目前为止，长链脂肪酸成为肥胖症即白色脂肪组织增生的配体，而过氧化物酶体增殖物激活受体（PPAR）作为一个主调节因子在转录水平上控制基因的揭示，开始在世界范围内迅速发现其功能受多种营养素进一步修饰的事实。在研究过氧化物酶体增殖物激活受体（PPAR）作为脂肪酸传感器的同时，对脂质代谢和能量代谢的影响也进行了深入的研究。 ...更多信息 ism相关基因的揭示是由某种信号传导机制控制的，无论是上述信号传导机制，还是受到膳食因素的修饰，对于能量交换系统功能发挥的可能性研究，是否会降低脂质代谢。我们分析了明确的3点作为研究目的，结果表明，控制转录的PPAR，本发明公开了一种脂质代谢和能量交换型基因的核转录因子配体，进而在该细胞核转录因子共激活因子信号转导系统中，特别是CREB连接蛋白（CBP）与PPAR配体过饱和的条件下，CBP显示量规定的代谢细节电子显示量在体内变得更清晰，如高脂、高脂食物摄入量，其中同系物p300有很深的参与。此外，它还存在于棕色脂肪组织中，并与与机体产热密切相关的辅激活蛋白（UCP）的偏离，揭示了脂肪代谢的降低。它是由过氧化物酶体增殖体激活受体（PPAR）控制的，与过氧化物酶体增殖体激活受体（PPAR）配体如高度不饱和脂肪酸和植物来源的类异戊二烯结合，提示了能量交换系统功能再现的可能性。少

项目成果

Takahashi N, et al.: "Abietic acid activates peroxisome proliferator-activated receptor-γ(PPARγ) in RAW264.7 macrophages and 3T3-L1 adipocytes to regulate gene expression involved in inflammation and lipid metabolism."FEBS Lett.. 550. 190-194 (2003)

Takahashi N 等人：“松香酸激活 RAW264.7 巨噬细胞和 3T3-L1 脂肪细胞中的过氧化物酶体增殖物激活受体 -γ (PPARγ)，以调节参与炎症和脂质代谢的基因表达。”FEBS Lett.. 550. 190 -194 (2003)

Takahashi N, et al.: "Dual action of isoprenols from herbal medicines on both PPARγ and PPARα in 3T3-L1 adipocytes and HepG2 hepatocytes."FEBS Lett.. 514. 315-322 (2002)

Takahashi N 等人：“草药中的异戊二烯醇对 3T3-L1 脂肪细胞和 HepG2 肝细胞中的 PPARγ 和 PPARα 的双重作用。”FEBS Lett.. 514. 315-322 (2002)

Takahashi N, Kawada T, Goto T, Yamamoto T, Taimatsu A, Matsui N, Kimura K, Saitoh M, Hosokawa M, Miya~hita K, Fushiki T.: "Dual action of isoprenols from herbal medicines on both PPARγ and. PPARα in 3T3-L1 adipocytes and HepG2. hepatocytes."FEBS Lett. 514

Takahashi N, Kawada T, Goto T, Yamamoto T, Taimatsu A, Matsui N, Kimura K, Saitoh M, Hosokawa M, Miya~hita K, Fushiki T.：“草药异戊二烯醇对 PPARγ 和 PPARα 的双重作用。在 3T3-L1 脂肪细胞和 HepG2 中。”FEBS Lett. 514。

Yu R, et al.: "Involvement of leukotactin-1, a novel CC chemokine, in human atherosclerosis"Atherosclerosi. (In press). (2004)

Yu R 等人：“一种新型 CC 趋化因子 leukotactin-1 在人类动脉粥样硬化中的参与”动脉粥样硬化。

Kim C.-S, et al.: "Macrophage inflammatory protein-related protein-2, a novel CC chemokine, can regulate preadipocyte migration and adipocyte differentiation."FEBS Lett.. 548. 125-130 (2003)

Kim C.-S 等人：“巨噬细胞炎症蛋白相关蛋白 2，一种新型 CC 趋化因子，可以调节前脂肪细胞迁移和脂肪细胞分化。”FEBS Lett.. 548. 125-130 (2003)