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首页> 外文期刊>Archives of Biological Sciences >NOVEL ACUTE STRESSOR EFFECTS ON INTERSCAPULAR BROWN ADIPOSE TISSUE SYMPATHETIC INERVATION AND UCP-1 CONTENT IN CHRONICALLY ISOLATED AND SPONTANEOUSLY HYPERTENSIVE RATS
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NOVEL ACUTE STRESSOR EFFECTS ON INTERSCAPULAR BROWN ADIPOSE TISSUE SYMPATHETIC INERVATION AND UCP-1 CONTENT IN CHRONICALLY ISOLATED AND SPONTANEOUSLY HYPERTENSIVE RATS

机译:慢性应激对慢性隔离和自发性高血压大鼠肋间褐脂肪组织交感神经和UCP-1含量的影响

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Interscapular brown adipose tissue (IBAT) is an energy storing organ involved in the maintenance of homeostasis in stress conditions when the balance of energy supplies is disturbed. The major regulator of IBAT activity is the sympathetic nervous system (SNS). Since genetic background is responsible for the individual differences in neuroendocrine stress responsivity, spontaneously hypertensive rats (SHR) that have a genetically increased general sympathetic output are a useful model for studying adaptive processes in stress conditions. Our aim was to test the effect of acute and/or chronic exposure to various stressors (thermal-cold, psychophysical-immobilization and psychosocial-isolation) on IBAT SNS and the metabolic activity in SHR, by measuring the number of monoamine-containing nerve endings and uncoupling protein-1 (UCP-1) content. The obtained results show that the IBAT SNS activity of unstressed SHR was stimulated by the administration of a single acute or chronic stressor and was independent of the duration or type of stressor, while chronic pre-stress of isolation suppressed further the SNS reaction to novel acute stress exposure. The IBAT UCP-1 content followed SNS changes, suggesting that this system is dominant in the regulation of IBAT metabolic rate in SHR.
机译:肩s间褐色脂肪组织(IBAT)是一种能量储存器官,当能量供应的平衡受到干扰时,它可以在压力条件下维持体内稳态。 IBAT活动的主要调节者是交感神经系统(SNS)。由于遗传背景是造成神经内分泌应激反应个体差异的原因,因此自发性高血压大鼠(SHR)具有遗传上增加的一般交感神经输出,是研究应激条件下适应性过程的有用模型。我们的目的是通过测量含单胺的神经末梢的数量,来测试急性和/或长期暴露于各种应激源(热,冷,心理物理固定和社会心理隔离)对IBAT SNS和SHR中代谢活性的影响。和解偶联蛋白1(UCP-1)的含量。获得的结果表明,通过施用单个急性或慢性应激源可以刺激未应激SHR的IBAT SNS活性,并且与应激源的持续时间或类型无关,而隔离的慢性预应激进一步抑制了SNS对新型急性应激的反应。压力暴露。 IBAT UCP-1含量随SNS变化而变化,表明该系统在SHR中IBAT代谢率的调节中占主导地位。

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