The Endless Summer: Thermoneutrality Prevents Monocytosis and Reduces Atherosclerosis.
The Endless Summer: Thermoneutrality Prevents Monocytosis and Reduces Atherosclerosis.
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DOI：
10.1161/circresaha.117.311721
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发表时间：
2017-09
影响因子：
20.1
通讯作者：
K. Woollard;A. Murphy
中科院分区：
文献类型：
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作者：
K. Woollard;A. Murphy
患有代谢综合征和肥胖症的人死于心血管疾病的风险增加。在过去的十年里，人们一直在深入研究刺激减肥以降低这种风险的新方法。其中一个关键组织是代谢活性棕色脂肪组织（BAT）。鉴于这是一种产热组织，它可以受到寒冷的刺激，并被一些人认为是减肥和改善人类健康其他方面的新前沿。但这对我们的动脉健康意味着什么呢？威廉姆斯等人在最新一期的《循环研究》中揭示，环境低温可能与我们的血管中的益处无关。通过比较在一系列温度下和2个动脉粥样硬化易感模型中动脉粥样硬化病变的发展，他们揭示了斑块大小的明显差异，因此在寒冷条件下的动物中发现了较大的病变。他们的研究揭示了一种新的温度敏感性调节单核细胞从骨髓中释放，最终影响动脉粥样硬化。重要的是，威廉姆斯等人1还解除了产热UCP 1（解偶联蛋白1）对动脉粥样硬化的代谢保护作用。文章，见662页长期以来，较冷的温度与心血管疾病的死亡率增加有关;然而，因果关系一直是间接的，传统危险因素的变化使其合理化（例如，血脂和血压）。2与此一致，Dong等人3最初发现冷住房（4°C）与热中性相比（不需要能量消耗来维持体温的温度）刺激BAT和白色脂肪组织的布朗宁。低温通过UCP 1引起脂解，导致致动脉粥样硬化脂蛋白水平升高。然而，环境温度和胆固醇的作用似乎存在争议，目前的研究报告没有变化。
People with metabolic syndrome and obesity are at an increased risk of mortality from cardiovascular disease. Over the past decade, there has been intensive research into new ways to stimulate weight loss to lower this risk. One of the key tissues is the metabolically active brown adipose tissue (BAT). Given that this is a thermogenic tissue, it can be stimulated by cold and is suggested by some as a new frontier in weight loss and improvements in other aspects of human health. But what does this mean for the health of our arteries? In the current issue of Circulation Research , Williams et al,1 reveal that ambient cool temperature may not correlate to benefit in our blood vessels. By comparing atherosclerotic lesion development over a series of temperatures and in 2 atherosclerotic prone models, they reveal stark differences in plaque size, such that larger lesions are found in animals under cold conditions. Their studies reveal a novel temperature-sensitive modulation of monocyte release from the bone marrow that ultimately impacts atherogenesis. Importantly, Williams et al1 have also uncoupled the metabolic protective role of the heat-generating UCP1 (uncoupling protein 1) from atherosclerosis. Article, see p 662 Cooler temperatures have long been associated with an increased mortality because of cardiovascular disease; however, the causality has been indirect, rationalized by changes in traditional risk factors (eg, lipids and blood pressure).2 In line with this, Dong et al3 originally found that cold housing (4°C) compared with thermoneutrality (the temperature at which energy expenditure is not needed to maintain body temperature) stimulated BAT and the browning of white adipose tissue. Cold temperature through UCP1 caused lipolysis and resulted in elevated levels of atherogenic lipoproteins. However, the role of ambient temperature and cholesterol seems controversial, with the current study reporting no changes.1 …