Different adaptive traits to cold exposure in young senescence-accelerated mice

Different adaptive traits to cold exposure in young senescence-accelerated mice
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DOI:
10.1007/s10522-005-3499-x
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发表时间:
2005
期刊:
影响因子:
4.5
通讯作者:
Y. Yamashita;Yoichi Chiba;Chen Xia;K. Hirayoshi;M. Satoh;Y. Saitoh;A. Shimada;E. Nakamura;M. Hosokawa
Y. Yamashita;Yoichi Chiba;Chen Xia;K. Hirayoshi;M. Satoh;Y. Saitoh;A. Shimada;E. Nakamura;M. Hosokawa
中科院分区:
医学3区
文献类型:
--
作者:
Y. Yamashita;Yoichi Chiba;Chen Xia;K. Hirayoshi;M. Satoh;Y. Saitoh;A. Shimada;E. Nakamura;M. Hosokawa

文献摘要

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对寒冷的适应能力降低是老年哺乳动物(包括人类)的一个显著特征。小鼠加速衰老倾向品系(SAMP)作为几种年龄相关疾病和加速衰老的动物模型进行了研究。最近的研究表明,SAMP菌株具有功能失调的过度活跃的线粒体,并且从年轻时起就处于较高的氧化应激状态。为了研究年轻的SAMP小鼠是否表现出寒冷适应能力受损,我们进行了冷暴露实验。在低温暴露期间,基线体温和最低体温没有应变差异。与SAMR1小鼠相比,SAMP1小鼠需要更长的时间才能达到最低温度。SAMR1小鼠在低温暴露后表现出体温升高,而SAMP1小鼠则没有。行为观察表明,在寒冷环境中,SAMP1小鼠比SAMR1小鼠运动更活跃。然而,与SAMR1小鼠相比,SAMP1小鼠的解偶联蛋白1(一种产热蛋白)mRNA水平以及血浆去甲肾上腺素水平更高。这一新发现的SAMP1小鼠生理表型为我们阐明加速衰老过程的遗传机制提供了工具,并有助于我们开发使人类健康老年的医学手段。
A reduced adaptation to cold is a prominent feature in aged mammals, including humans. The accelerated senescence-prone strain of mice (SAMP) has been studied as an animal model for several age-associated disorders and in the acceleration of senescence. Recent studies revealed that SAMP strains have dysfunctional hyperactive mitochondria and are under a higher oxidative stress status from a young age. To investigate whether young SAMP mice show impaired cold adaptation abilities, we performed cold-exposure experiments. There were no strain differences in baseline body temperature and lowest reached temperature during cold exposure. SAMP1 mice took longer times to reach their lowest temperature in comparison to SAMR1 mice. SAMR1 mice showed an elevation in temperature following cold exposure, whereas SAMP1 mice did not. Behavioral observations demonstrated that SAMP1 mice moved more actively than SAMR1 during cold exposure. However, mRNA levels of uncoupling protein 1 (UCP1), a heat generating protein, as well as plasma norepinephrine levels, were higher in SAMP1 than in SAMR1 mice. This newly found physiological phenotype in SAMP1 mice provides us with a tool to clarify the genetic mechanism which accelerates the senescence process and helps us develop medical means which will bring mankind to a healthy old age.