After a cold conditioning swim, UCP2-deficient mice are more able to defend against the cold than wild type mice.

After a cold conditioning swim, UCP2-deficient mice are more able to defend against the cold than wild type mice.
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DOI:
10.1016/j.physbeh.2014.06.014
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发表时间:
2014-08
影响因子:
2.9
通讯作者:
Larson AA
Larson AA
中科院分区:
医学3区
文献类型:
--
作者:
Abdelhamid RE;Kovács KJ;Nunez MG;Larson AA

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解偶联蛋白2 (Uncoupling protein 2, UCP2)广泛分布于全身,包括大脑、脂肪组织和骨骼肌。与UCP1相反,UCP2不影响静息体温,UCP2缺陷(-/-)小鼠对单次暴露于寒冷环境温度有正常的体温调节反应。相反,缺乏ucp2的小鼠比野生型小鼠更焦虑,表现出快感缺乏,循环皮质酮水平更高。为了测试UCP2在抑郁行为中的可能作用,我们将UCP2缺陷小鼠和野生型小鼠暴露在寒冷(26°C)的强迫游泳中,同时测量游泳期间和游泳后的直肠温度。ucp2缺失小鼠的静止时间与野生型小鼠没有差异,所有小鼠在第2天都漂浮得更多。然而,与野生型小鼠相比,ucp2缺陷小鼠在26°C下进行第二次每日游泳时抵御体温下降的能力更强(野生型小鼠曲线下面积:247.0±6.4;ucp2缺陷小鼠:284.4±3.8,P<0.0001,学生t检验)。野生型小鼠在26°C下第二次游泳时体温调节的改善与它们更大的不动性相关,而在41°C下游泳时对体温的防御与ucp2缺陷小鼠更大的不动性相关。综上所述,这些数据表明,虽然缺乏UCP2对体温没有急性影响,但与UCP1相反,UCP2可能会抑制抵御寒冷的快速改善,而UCP1的主要功能是促进产热。
Uncoupling protein 2 (UCP2) is widely distributed throughout the body including the brain, adipose tissue and skeletal muscles. In contrast to UCP1, UCP2 does not influence resting body temperature and UCP2-deficient (-/-) mice have normal thermoregulatory responses to a single exposure to cold ambient temperatures. Instead, UCP2-deficient mice are more anxious, exhibit anhedonia and have higher circulating corticosterone than wild type mice. To test the possible role of UCP2 in depressive behavior we exposed UCP2-deficient and wild type mice to a cold (26°C) forced swim and simultaneously measured rectal temperatures during and after the swim. The time that UCP2-deficient mice spent immobile did not differ from wild type mice and all mice floated more on day 2. However, UCP2-deficient mice were more able to defend against the decrease in body temperature during a second daily swim at 26°C than wild type mice (area under the curve for wild type mice: 247.0 ± 6.4; for UCP2-deficient mice: 284.4 ± 3.8, P<0.0001, Student's t test). The improved thermoregulation of wild type mice during a second swim at 26°C correlated with their greater immobility whereas defense against the warmth during a swim at 41°C correlated better with greater immobility of UCP2-deficient mice. Together these data indicate that while the lack of UCP2 has no acute effect on body temperature, UCP2 may inhibit rapid improvements in defense against cold, in contrast to UCP1, whose main function is to promote thermogenesis.
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发表时间: 2013-09
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