Fyda D M, Cooper K E, Veale W L
Department of Medical Physiology, Faculty of Medicine, University of Calgary, Alta., Canada.
Brain Res. 1991 Apr 19;546(2):203-10. doi: 10.1016/0006-8993(91)91482-g.
Given that relatively little is known regarding the central control of brown adipose tissue (BAT)-mediated thermogenesis the present study assessed whether the direct pharmacological stimulation of beta- or alpha-adrenergic receptors located on the brown adipocytes would result in a typical thermogenic response following electrolytic lesions to the nucleus tractus solitarius (NTS). Bilateral electrolytic lesions to the NTS in the rat effectively disrupted the baroreceptor reflex arc. It was observed that the metabolic and temperature responses to either norepinephrine (1, 5, or 25 micrograms/kg/min) or to the beta-agonist isoproterenol (0.5 micrograms/kg/min) were significantly attenuated in the NTS-lesioned rats relative to the control animals with an intact baroreflex. Conversely, the cardiovascular effects of norepinephrine or of the alpha-agonist phenylephrine (10 micrograms/kg/min) were enhanced in the NTS-lesioned animals. The results suggest that the functional capacity of the brown adipocytes was reduced following NTS lesions and points to an alteration in the ability of beta-receptors to respond to pharmacological stimulation with a typical thermogenic response.
鉴于目前对棕色脂肪组织(BAT)介导的产热的中枢控制了解相对较少,本研究评估了对棕色脂肪细胞上的β-或α-肾上腺素能受体进行直接药理刺激是否会在对孤束核(NTS)进行电解损伤后引发典型的产热反应。对大鼠的NTS进行双侧电解损伤有效地破坏了压力感受器反射弧。观察到,与具有完整压力反射的对照动物相比,NTS损伤大鼠对去甲肾上腺素(1、5或25微克/千克/分钟)或β-激动剂异丙肾上腺素(0.5微克/千克/分钟)的代谢和温度反应明显减弱。相反,在NTS损伤的动物中,去甲肾上腺素或α-激动剂去氧肾上腺素(10微克/千克/分钟)的心血管效应增强。结果表明,NTS损伤后棕色脂肪细胞的功能能力降低,这表明β-受体对典型产热反应的药理刺激的反应能力发生了改变。