Thermoneutrality decreases thermogenic program and promotes adiposity in high-fat diet-fed mice.
Thermoneutrality decreases thermogenic program and promotes adiposity in high-fat diet-fed mice.
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DOI：
10.14814/phy2.12799
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发表时间：
2016-05
影响因子：
2.5
通讯作者：
Xue B
中科院分区：
文献类型：
--
作者：
Cui X;Nguyen NL;Zarebidaki E;Cao Q;Li F;Zha L;Bartness T;Shi H;Xue B
棕色/米色脂肪细胞是对抗肥胖的治疗靶点，因为它们能够通过适应性产热耗散能量。大多数研究棕色/米色脂肪细胞的诱导的研究在冷条件下进行（例如，4°C）;关于棕色/米色脂肪细胞的产热程序如何在热中性条件下被调节（例如，30°C），这在日常生活中人类住宅的热舒适区内。因此，本研究旨在表征在环境温度（22°C）与热中性条件（30°C）下饲养的小鼠中棕色/米色脂肪细胞的产热程序。在22°C或30°C下饲养的雄性小鼠喂食普通饲料或高脂肪（HF）饲料20周。尽管食物摄入较少，但与22°C下的小鼠相比，30°C下饲养的食物喂养的小鼠保持相同的体重。然而，这些热中性圈养的小鼠在具有较大脂肪细胞的棕色和白色脂肪库中显示产热程序表达的减少。当用普通饲料配对喂养时，热中和饲养的小鼠显示体重增加。此外，热中性增加用HF饮食喂养的小鼠的体重。这与在热中性饲养小鼠的棕色和白色脂肪库中产热程序的表达降低有关。产热程序的下调可能是由于热中性饲养小鼠的交感神经驱动力降低所致，这一点通过棕色和白色脂肪库中酪氨酸羟化酶表达和去甲肾上腺素周转率的降低而得到证实。我们的数据表明，热中性可能负调节产热程序和交感神经驱动，导致增加肥胖的小鼠。
Brown/beige adipocytes are therapeutic targets to combat obesity due to their abilities to dissipate energy through adaptive thermogenesis. Most studies investigating induction of brown/beige adipocytes were conducted in cold condition (e.g., 4°C); much is unknown about how the thermogenic program of brown/beige adipocytes is regulated in thermoneutral condition (e.g., 30°C), which is within the thermal comfort zone of human dwellings in daily life. Therefore, this study aims to characterize the thermogenic program of brown/beige adipocytes in mice housed under ambient (22°C) versus thermoneutral condition (30°C). Male mice raised at 22°C or 30°C were fed either chow diet or high‐fat (HF) diet for 20 weeks. Despite less food intake, chow‐fed mice housed at 30°C remained the same body weight compared to mice at 22°C. However, these thermoneutrally housed mice displayed a decrease in the expression of thermogenic program in both brown and white fat depots with larger adipocytes. When pair‐fed with chow diet, thermoneutrally housed mice showed an increase in body weight. Moreover, thermoneutrality increased body weight of mice fed with HF diet. This was associated with decreased expression of the thermogenic program in both brown and white fat depots of the thermoneutrally housed mice. The downregulation of the thermogenic program might have resulted from decreased sympathetic drive in the thermoneutrally housed mice evident by decreased expression of tyrosine hydroxylase expression and norepinephrine turnover in both brown and white fat depots. Our data demonstrate that thermoneutrality may negatively regulate the thermogenic program and sympathetic drive, leading to increased adiposity in mice.