An Adipocyte-specific Plasma Protein, Adiponectin/GBP28, functions as a mediator of biological defense mechanism.

脂联素/GBP28 是一种脂肪细胞特异性血浆蛋白,可作为生物防御机制的介质。

基本信息

项目摘要

Recently, adiponectin/GBP28, a plasma protein which is specifically endocrined with adipose tissue, has been found to have the activities that decreased plasma fatty acids concentration and improve insulin resistance. These activities indicate that adiponectin/GBP28 relates to metabolic syndrome.In this study, we produced adiponectin/GBP28-transgenic mice (Tg) and anti-transgenic mice (anti-Tg) to investigate whether adiponectin plays a role in regulation of energy homeostasis. While the wild mice expressed adiponectin/GBP28 in adipose tissue only, Tg mice expressed the protein in all tissues. The plasma concentration of adiponectin/GBP28 of Tg mice was higher than that of wild mice during juvenile stage and decreased in the same level as that of wild mice as they grow ; that of anti-Tg mice was always less than that of wild mice. It is notable that mature female mice changed the plasma concentration of adiponectin/GBP28 under the cycle of menstrual period.Under fasting conditions, anti-Tg mice decreased their body weight faster than wild and Tg mice. Interestingly, the anti-Tg mice tended to die after 48-hr fasting. We also found that the anti-Tg mice significantly reduced locomotion activities and body temperature after 48-hr fasting. Intestinal bleeding which might be caused by bacterial attacking seemed to be the cause of the anti-Tg mice's death. The findings suggested that adiponectin/GBP28 plays a role in biological defense systems as well as regulation of lipid metabolism. Thus, a possibility was considered that the deletion of adiponectin/GBP28 decreased a regulatory response against the changes of environmental conditions.When anti-Tg mice were exposed under cold circumstance at 5℃, the anti-Tg mice decreased their body temperature faster than wild mice. This results support that the deletion of adiponectin/GBP28 caused the disorder of lipid metabolism to maitain body temperature.
最近发现脂联素/GBP28是一种脂肪组织特异性内分泌的血浆蛋白,具有降低血浆脂肪酸浓度和改善胰岛素抵抗的活性。这些活性表明脂联素/GBP28与代谢综合征有关。在本研究中,我们制备了脂联素/GBP28转基因小鼠(Tg)和抗转基因小鼠(抗-Tg),以研究脂联素是否在能量稳态调节中发挥作用。野生小鼠仅在脂肪组织中表达脂联素/GBP28,而 Tg 小鼠在所有组织中表达该蛋白。 Tg小鼠的血浆脂联素/GBP28浓度在幼年期高于野生小鼠,随着生长过程的降低与野生小鼠相同水平;抗-Tg小鼠的结果始终低于野生小鼠。值得注意的是,成熟雌性小鼠在月经周期中血浆脂联素/GBP28浓度发生变化。在禁食条件下,抗Tg小鼠的体重下降速度快于野生小鼠和Tg小鼠。有趣的是,抗 Tg 小鼠在禁食 48 小时后往往会死亡。我们还发现,禁食 48 小时后,抗​​ Tg 小鼠的运动活动和体温显着降低。可能由细菌攻击引起的肠道出血似乎是抗Tg小鼠死亡的原因。研究结果表明脂联素/GBP28 在生物防御系统以及脂质代谢调节中发挥作用。因此,认为脂联素/GBP28的缺失降低了对环境条件变化的调节反应。当抗Tg小鼠暴露在5℃的寒冷环境中时,抗Tg小鼠比野生小鼠更快地降低体温。这一结果支持脂联素/GBP28的缺失导致维持体温的脂质代谢紊乱。

项目成果

期刊论文数量(8)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
タンパク質構造からみたアディポネクチンの生理活性予測
从蛋白质结构预测脂联素的生理活性
  • DOI:
  • 发表时间:
    2004
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Junko Sugatani;et al.;富田 基郎
  • 通讯作者:
    富田 基郎
Increased serum leptin protects from adiposity despite the increased glucose uptake in white adipose tissue in mice lacking p85alpha phosphoinositide 3-kinase.
  • DOI:
    10.2337/diabetes.53.9.2261
  • 发表时间:
    2004-09
  • 期刊:
  • 影响因子:
    7.7
  • 作者:
    Y. Terauchi;J. Matsui;J. Kamon;T. Yamauchi;N. Kubota;K. Komeda;S. Aizawa;Y. Akanuma;Motowo Tomita;T. Kadowaki
  • 通讯作者:
    Y. Terauchi;J. Matsui;J. Kamon;T. Yamauchi;N. Kubota;K. Komeda;S. Aizawa;Y. Akanuma;Motowo Tomita;T. Kadowaki
{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ monograph.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ sciAawards.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ conferencePapers.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ patent.updateTime }}

TOMITA Motowo其他文献

TOMITA Motowo的其他文献

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

{{ truncateString('TOMITA Motowo', 18)}}的其他基金

Characterization of physiological function of the plasma proteins, PFBP and IHRP with knockout mice.
敲除小鼠血浆蛋白、PFBP 和 IHRP 生理功能的表征。
  • 批准号:
    11470489
  • 财政年份:
    1999
  • 资助金额:
    $ 2.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Biological functions of novel human plasma proteins, IHRP and PHBP.
新型人血浆蛋白 IHRP 和 PHBP 的生物学功能。
  • 批准号:
    08457615
  • 财政年份:
    1996
  • 资助金额:
    $ 2.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Devlopment of MACIF as a new medicine for regulation of membrane attack complex of complement
MACIF作为调节补体膜攻击复合物的新药的开发
  • 批准号:
    02557103
  • 财政年份:
    1990
  • 资助金额:
    $ 2.3万
  • 项目类别:
    Grant-in-Aid for Developmental Scientific Research (B)
Search of a gene family containing MACIF, a regulatory membrane protein of complement system
补体系统调节膜蛋白MACIF基因家族的寻找
  • 批准号:
    02454487
  • 财政年份:
    1990
  • 资助金额:
    $ 2.3万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
Structural analysis of regulatory factors of complement on erythrocyte membranes
红细胞膜上补体调节因子的结构分析
  • 批准号:
    62580132
  • 财政年份:
    1987
  • 资助金额:
    $ 2.3万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
Recognition mechanism of heterologous erythrocytes by the alternative pathway of complement.
补体旁路途径对异源红细胞的识别机制。
  • 批准号:
    59580109
  • 财政年份:
    1984
  • 资助金额:
    $ 2.3万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了