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[体温调节性产热的调节]

[Regulation of thermoregulatory thermogenesis].

作者信息

Kuroshima A

机构信息

First Department of Physiology, Asahikawa Medical College, Japan.

出版信息

Hokkaido Igaku Zasshi. 1995 Jan;70(1):1-8.

PMID:7744360
Abstract

Two modes of heat production exist which are involved in body temperature regulation with decreasing environmental temperature: shivering thermogenesis and more efficient nonshivering thermogenesis (NST). Enhanced NST is mediated by the activated sympathetic nervous activity and increased secretions of hormonal factors such as glucagon through an enhanced lipid utilization. Moreover, cold acclimation causes an increased responsiveness of the organism to these factors. Noradrenaline-induced secretion of glucagon is also enhanced by cold acclimation. Chronic administration of glucagon simulates cold acclimation, resulting in an improved cold tolerance by an increased NST. Brown adipose tissue (BAT) is a major site for nonshivering thermogenesis (NST) during metabolic cold acclimation. Cold acclimation causes a hyperplasia as well as an enhanced metabolic capacity of BAT cell. BAT function is mainly regulated by sympathetic noradrenaline and several hormonal factors such as glucagon. BAT possesses rich blood supply by which its high thermogenic capacity and an efficient transfer of heat are maintained. Noradrenaline and glucagon increases not only heat production, but also blood flow in BAT. Nitric oxide (NO), endothelium-derived relaxing factor, is involved in noradrenaline-, glucagon- and cold-induced increases of blood flow through BAT. Noradrenaline-induced BAT thermogenesis is suggested to be mediated by NO. NO synthase occurs in BAT cell in addition to endothelium of BAT vessel. These findings indicate that NO may be a signalling molecule for an enhanced NST during cold acclimation. Moreover, BAT contributes to adaptation to overfeeding, nonthermal stress and fever by means of producing heat, playing a role as adaptive organ in overall energy metabolism.

摘要

随着环境温度降低,存在两种参与体温调节的产热方式:寒颤产热和效率更高的非寒颤产热(NST)。增强的NST由激活的交感神经活动介导,并通过增强脂质利用增加胰高血糖素等激素因子的分泌。此外,冷适应会导致机体对这些因素的反应性增加。冷适应还会增强去甲肾上腺素诱导的胰高血糖素分泌。长期给予胰高血糖素可模拟冷适应,通过增加NST提高耐寒性。棕色脂肪组织(BAT)是代谢性冷适应期间非寒颤产热(NST)的主要部位。冷适应会导致BAT细胞增生以及代谢能力增强。BAT功能主要受交感去甲肾上腺素和胰高血糖素等几种激素因子调节。BAT拥有丰富的血液供应,借此维持其高产热能力和有效的热量传递。去甲肾上腺素和胰高血糖素不仅会增加产热,还会增加BAT中的血流量。一氧化氮(NO),即内皮源性舒张因子,参与去甲肾上腺素、胰高血糖素和寒冷诱导的通过BAT的血流量增加。去甲肾上腺素诱导的BAT产热被认为是由NO介导的。除了BAT血管内皮外,BAT细胞中也存在一氧化氮合酶。这些发现表明,NO可能是冷适应期间增强NST的信号分子。此外,BAT通过产热有助于适应过度喂养、非热应激和发热,在整体能量代谢中作为适应性器官发挥作用。

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