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Sites and cellular mechanisms of human adrenergic thermogenesis - a review [Review]

机译:肾上腺素能热生成的部位和细胞机制-综述[综述]

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Nonshivering thermogenesis (NST) is considered to be an important physiological mechanism, which contributes to the maintenance of the heat balance in cold exposed mammals. Numerous studies confirmed the role of noradrenaline released from the sympathetic nervous system and the significance of #beta#_3-adrenergic cell membrane receptors and mitochondrial uncoupling proteins in mediation of NST in rodents. Furthermore, the literature documents sample evidence that NST can be potentiated in cold adapted mammals that increased their survival limits considerably. It has been shown that NST plays a significant role mainly in small mammals. In species bigger than about 10kg its physiological significance appears to be questionable and in humans a role in the maintenance of heat balance is still to be precisely established (Jansky, 1995). It has also been suggested that NST plays a role in the maintenance of heat balance even under thermoneutral conditions. Defective heat production mechanisms may lower energy expenditure during diet-induced thermogenesis and, consequently, may be one of the reasons of obesity. Evidence exists that in obese subjects a reduced response to adrenomimetics (Jung et al., 1979; Vybiral et al., 2000a, b), mutation of the fi3-adrenoceptor gene (Yoshida and Sakane, 1999) and uncoupling protein polymorphism (Walder et al., 1998) are found. In consequence, studies on NST in humans could be of considerable practical importance and could contribute to explaining various problems of pathophysiology of thermoregulation. The purpose of this review is to discuss the evidence that thermoregulatory NST also functions in humans and that the cellular mechanisms of human NST differ from those found in small mammals. It is also possible that metabolic rate (MR) can be regulated by physiological processes at the organ level as well as by biochemical mechanisms (Kolar and Jansky, 1984a, b; Clark et al., 1994, 1995), new approaches to the problem appear to be desirable.
机译:不发抖的生热(NST)被认为是重要的生理机制,有助于维持受冷暴露的哺乳动物的热量平衡。大量研究证实了从交感神经系统释放的去甲肾上腺素的作用以及#beta#_3-肾上腺能细胞膜受体和线粒体解偶联蛋白在NST介导啮齿类动物中的意义。此外,文献文献证据表明,NST可以在适应寒冷的哺乳动物中增强,从而大大提高其生存极限。已经表明,NST主要在小型哺乳动物中起重要作用。在大于约10kg的物种中,其生理学意义似乎值得怀疑,而在人类中,维持热量平衡的作用仍需精确确定(Jansky,1995)。也有人提出,即使在热中性条件下,NST在维持热量平衡中也起着作用。热量产生机制不良可能会降低饮食引起的热量生成过程中的能量消耗,因此可能是肥胖的原因之一。有证据表明,在肥胖的受试者中,对肾上腺模拟物的反应减少(Jung等,1979; Vybiral等,2000a,b),fi3-肾上腺素能受体基因的突变(Yoshida和Sakane,1999)和蛋白多态性脱钩(Walder等)。等(1998)。因此,对人类NST的研究可能具有相当大的实际意义,并且可能有助于解释温度调节的病理生理学的各种问题。这篇综述的目的是讨论温度调节性NST在人类中也起作用的证据,以及人类NST的细胞机制与在小型哺乳动物中发现的不同。也有可能通过器官一级的生理过程和生化机制来调节代谢率(MR)(Kolar和Jansky,1984a,b; Clark等,1994,1995),这是解决该问题的新方法。似乎是可取的。

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