Housing temperature affects the acute and chronic metabolic adaptations to exercise in mice
Housing temperature affects the acute and chronic metabolic adaptations to exercise in mice
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DOI：
10.1113/jp278221
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发表时间：
2019-07-11
影响因子：
5.5
通讯作者：
Wright, David C.
中科院分区：
文献类型：
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作者：
McKie, Greg L.;Medak, Kyle D.;Wright, David C.
关键点小鼠通常被安置在低于其热中性区的室温下，这意味着它们暴露在慢性热应激中。耐力运动诱导啮齿类动物白色脂肪组织的布朗宁和线粒体生物合成，但在人类中有相互矛盾的报道。我们假设，小鼠所处的环境室温可以部分解释人类和啮齿动物之间的这些不一致的报告。我们将小鼠置于室温或热中性环境中，研究它们对急性和慢性运动的生理反应。我们发现，热中性住房改变了运行行为和葡萄糖稳态，并进一步，运动诱导的线粒体生物合成和白色脂肪组织的布朗宁的标记物在热中性住房小鼠减少。小鼠通常被饲养在低于其热中性区的温度下，导致产热的补偿性增加。尽管如此，许多研究报告将小鼠置于室温（RT）下，可能是为了方便研究人员研究它们。因此，人类和啮齿类动物之间关于运动增加白色脂肪组织中线粒体和产热标记物的能力的相互矛盾的报告可以通过经常被忽视的变量来解释，即房屋温度。为了验证这一假设，我们将雄性C57 BL/6小鼠在RT（22 ℃）或热中性（TN）（29 ℃）下饲养6周，有或没有获得自主跑步轮，或使它们进行急性力竭的跑步机跑步。我们检测了骨骼肌、附睾白色脂肪组织（eWAT）、腹股沟白色脂肪组织（iWAT）和棕色脂肪组织（BAT）中选择的线粒体和产热标志物的基因表达和蛋白质含量。我们还评估了脂肪细胞形态和葡萄糖稳态指数。房屋温度影响体内葡萄糖耐量和胰岛素作用，但无论是急性还是慢性运动的有益效果，在eWAT，BAT和骨骼肌中保持完整，与房屋温度无关。在TN饲养小鼠导致运动对iWAT的一些影响减弱。总的来说，我们目前的数据特征的急性和慢性代谢适应运动在不同的住房温度和证明，第一次，温度影响运动的能力，以增加线粒体生物合成和布朗宁的标志物的白色脂肪组织。
Key pointsMice are commonly housed at room temperatures below their thermoneutral zone meaning they are exposed to chronic thermal stress. Endurance exercise induces browning and mitochondrial biogenesis in white adipose tissue of rodents, but there are conflicting reports of this phenomenon in humans. We hypothesized that the ambient room temperature at which mice are housed could partially explain these discrepant reports between humans and rodents. We housed mice at room temperature or thermoneutrality and studied their physiological responses to acute and chronic exercise. We found that thermoneutral housing altered running behaviour and glucose homeostasis, and further, that exercise-induced markers of mitochondrial biogenesis and the browning of white adipose tissue were reduced in mice housed at thermoneutrality. Mice are often housed at temperatures below their thermoneutral zone resulting in compensatory increases in thermogenesis. Despite this, many studies report housing mice at room temperature (RT), likely for the convenience of the researchers studying them. As such, the conflicting reports between humans and rodents regarding the ability of exercise to increase mitochondrial and thermogenic markers in white adipose tissue may be explained by the often-overlooked variable, housing temperature. To test this hypothesis, we housed male C57BL/6 mice at RT (22 degrees C) or thermoneutrality (TN) (29 degrees C) with or without access to a voluntary running wheel for 6 weeks or subjected them to an acute exhaustive bout of treadmill running. We examined the gene expression and protein content of select mitochondrial and thermogenic markers in skeletal muscle, epididymal white adipose tissue (eWAT), inguinal white adipose tissue (iWAT) and brown adipose tissue (BAT). We also assessed adipocyte morphology and indices of glucose homeostasis. Housing temperature influenced glucose tolerance and insulin action in vivo, yet the beneficial effects of exercise, both acute and chronic, remained intact in eWAT, BAT and skeletal muscle irrespective of housing temperature. Housing mice at TN led to an attenuation of some of the effects of exercise on iWAT. Collectively, we present data characterizing the acute and chronic metabolic adaptations to exercise at different housing temperatures and demonstrate, for the first time, that temperature influences the ability of exercise to increase markers of mitochondrial biogenesis and the browning of white adipose tissue.