重新审视非颤抖产热:交感和非交感贡献

Orien L Tulp
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摘要

饮食和环境因素构成了影响人类和动物饮食诱导产热量的互补、叠加机制。短期交感神经介导和长效甲状腺介导的途径都已被确定,并以代谢协调的方式发挥作用,促进营养过剩和营养不足期间涉及多个器官和外周组织的能量平衡的生化和生理途径。在一个已知表达环境和饮食诱导的产热参数的同源瘦啮齿动物模型中,在安静休息的动物在摄入高能量美味饮食后,甲状腺和交感神经分别贡献了大约50%的相对VO2增加,这是通过α-甲基副酪氨酸(一种交感神经麻痹化学剂)的存在和不存在来确定的。相反,在肥胖和其他啮齿类动物的肥胖表型中,在营养和环境挑战的影响下,交感神经和甲状腺对适应性产热机制的贡献都受到了损害,从而导致能量代谢和体脂肪增加的效率更高。因此,本综述的目的是近似确定与正常瘦型大鼠LA/Ntul//-cp中饮食诱导产热表达的生理过程相关的两个主要因素之间的定性分布。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nonshivering thermogenesis revisited: sympathetic and non-sympathetic contributions
Factors of diet and environment contribute to complementary, additive mechanisms that influence the magnitude of diet induced thermogenesis generated in man and animals. Both short terms sympathetically mediated and longer acting thyroidal mediated pathways have been identified and appear to function in a metabolically coordinated fashion to facilitate biochemical and physiologic pathways of energy balance implicating multiple organs and peripheral tissues during periods of over- and under-nutrition. In a congenic lean rodent model known to express parameters of environmentally and diet induced mediated thermogenesis, thyroidal and sympathetic contributions each contributed to approximately 50% of the relative increase in VO2 in quietly resting animals after consuming a high energy palatable diet as determined in the presence vs. absence of α-methylparatyrosine, a sympathoplegic chemical agent. In contrast, in the obese phenotype of the corpulent and other rodent strains, both sympathetic and thyroidal contributions to adaptive thermogenic mechanisms are impaired in response to both nutritional and environmental challenge, contributing to a greater efficiency of energy metabolism and body fat accretion. Thus, the purpose of the present review is to approximate the qualitative distribution between the two primary factors linked to the physiologic process resulting in the expression of diet induced thermogenesis in a normally lean phenotype of rat, the LA/Ntul//-cp.
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