PDF(Pubmed)
Abstract：
OBJECTIVE: Preserving core body temperature across a wide range of ambient temperatures requires adaptive changes of thermogenesis that must be offset by corresponding changes of energy intake if body fat stores are also to be preserved. Among neurons implicated in the integration of thermoregulation with energy homeostasis are those that express both neuropeptide Y (NPY) and agouti-related protein (AgRP) (referred to herein as AgRP neurons). Specifically, cold-induced activation of AgRP neurons was recently shown to be required for cold exposure to increase food intake in mice. Here, we investigated how consuming a high-fat diet (HFD) impacts various adaptive responses to cold exposure as well as the responsiveness of AgRP neurons to cold.
METHODS: To test this, we used immunohistochemistry, in vivo fiber photometry and indirect calorimetry for continuous measures of core temperature, energy expenditure, and energy intake in both chow- and HFD-fed mice housed at different ambient temperatures.
RESULTS: We show that while both core temperature and the thermogenic response to cold are maintained normally in HFD-fed mice, the increase of energy intake needed to preserve body fat stores is blunted, resulting in weight loss. Using both immunohistochemistry and in vivo fiber photometry, we show that although cold-induced AgRP neuron activation is detected regardless of diet, the number of cold-responsive neurons appears to be blunted in HFD-fed mice.
CONCLUSIONS: We conclude that HFD-feeding disrupts the integration of systems governing thermoregulation and energy homeostasis that protect body fat mass during cold exposure.
METHODS: To test this, we used immunohistochemistry, in vivo fiber photometry and indirect calorimetry for continuous measures of core temperature, energy expenditure, and energy intake in both chow- and HFD-fed mice housed at different ambient temperatures.
RESULTS: We show that while both core temperature and the thermogenic response to cold are maintained normally in HFD-fed mice, the increase of energy intake needed to preserve body fat stores is blunted, resulting in weight loss. Using both immunohistochemistry and in vivo fiber photometry, we show that although cold-induced AgRP neuron activation is detected regardless of diet, the number of cold-responsive neurons appears to be blunted in HFD-fed mice.
CONCLUSIONS: We conclude that HFD-feeding disrupts the integration of systems governing thermoregulation and energy homeostasis that protect body fat mass during cold exposure.
摘要：
目的：在广泛的环境温度范围内保持核心体温需要热生成的适应性变化，如果要保持体内脂肪储存，则必须通过相应的能量摄入变化来抵消。在涉及体温调节与能量稳态的整合的神经元中,是表达神经肽Y(NPY)和刺鼠相关蛋白(AgRP)两者的那些神经元(本文称为AgRP神经元)。具体来说,冷诱导的AgRP神经元的激活最近被证明是冷暴露所必需的，以增加小鼠的食物摄入量。这里,我们调查了高脂饮食(HFD)如何影响各种对冷暴露的适应性反应以及AgRP神经元对冷的反应.
方法：要对此进行测试，我们用免疫组织化学,用于连续测量核心温度的体内纤维光度法和间接量热法，能量消耗，以及在不同环境温度下饲养的chow和HFD喂养的小鼠的能量摄入。
结果：我们表明，尽管在喂食HFD的小鼠中，核心温度和对寒冷的热原反应均正常维持，保持体内脂肪储存所需的能量摄入的增加被减弱，导致体重减轻。使用免疫组织化学和体内纤维光度法，我们表明，尽管冷诱导的AgRP神经元激活被检测到与饮食无关，在HFD喂养的小鼠中,冷响应神经元的数量似乎减弱。
结论：我们得出结论，HFD喂养破坏了控制体温调节和能量稳态的系统的整合，从而在寒冷暴露期间保护身体脂肪量。
方法：要对此进行测试，我们用免疫组织化学,用于连续测量核心温度的体内纤维光度法和间接量热法，能量消耗，以及在不同环境温度下饲养的chow和HFD喂养的小鼠的能量摄入。
结果：我们表明，尽管在喂食HFD的小鼠中，核心温度和对寒冷的热原反应均正常维持，保持体内脂肪储存所需的能量摄入的增加被减弱，导致体重减轻。使用免疫组织化学和体内纤维光度法，我们表明，尽管冷诱导的AgRP神经元激活被检测到与饮食无关，在HFD喂养的小鼠中,冷响应神经元的数量似乎减弱。
结论：我们得出结论，HFD喂养破坏了控制体温调节和能量稳态的系统的整合，从而在寒冷暴露期间保护身体脂肪量。
