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首页> 美国卫生研究院文献>British Journal of Pharmacology and Chemotherapy >Sympathetic mechanisms in diet-induced thermogenesis: modification by ciclazindol and anorectic drugs.
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Sympathetic mechanisms in diet-induced thermogenesis: modification by ciclazindol and anorectic drugs.

机译：饮食诱导生热的交感机制：ciclazindol和厌食药修饰。

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1 The sympathetic noradrenergic activation of brown adipose tissue and the biochemical mechanisms involved in diet-induced thermogenesis were studied in rats. 2 A close correlation was found between brown adipose tissue Na+, K+-adenosinetriphosphatase (Na+, K+-ATPase) activity in vitro and in vivo measurements of resting oxygen consumption (VO2). The effects of noradrenaline on in vitro NA+, K+-ATPase activity in brown adipose tissue and in vivo VO2 could be mimicked by a variety of agents. These included beta-adrenoceptor agonists and agents known to induce the release of noradrenaline or inhibit the noradrenaline uptake process. The pharmacological evidence suggests that dopaminergic mechanisms may also be involved in the control of thermogenesis. 3 Amphetamine did not increase VO2 in rats without causing associated increases in locomotor activity. Ciclazindol at doses of 3-30 mg/kg intraperitoneally increased VO2 but did not appear to increase locomotor activity or evoke any other signs of CNS stimulation including lengthening of time to sleep onset or stereotypy. Separation of metabolic and CNS effects occurred only at the lowest dose of mazindol used (0.3 mg/kg i.p.). These results are probably a reflection of (a) the relative abilities of these drugs to inhibit brain and brown adipose noradrenaline uptake processes and (b) the relatively high accumulation of ciclazindol in brown adipose. 4 Of the drugs tested, only ciclazindol was a more potent inhibitor of the noradrenaline uptake system in brown adipose tissue (BAT) than in brain. Kinetic analysis also revealed that the actions of ciclazindol on the NA uptake system and Na+, K+-ATPase in BAT differed from those of mazindol. 5 These findings suggest that ciclazindol may produce an energy wasting effect in rodents without causing overt CNS stimulation; the implications of these findings in terms of human obesity are discussed.
机译：1在大鼠中研究了棕色脂肪组织的交感性去甲肾上腺素能激活及其与饮食诱导的生热有关的生化机制。 2发现棕色脂肪组织的Na +，K +-腺苷三磷酸酶（Na +，K + -ATPase）活性与体内静息耗氧量（VO2）的测量密切相关。去甲肾上腺素对棕色脂肪组织中的NA +，K + -ATPase活性和体内VO2的影响可以通过多种药物来模拟。这些包括β-肾上腺素受体激动剂和已知诱导去甲肾上腺素释放或抑制去甲肾上腺素摄取过程的药物。药理证据表明，多巴胺能机制也可能参与生热的控制。 3苯丙胺不会增加大鼠的VO2，而不会引起运动活性的增加。腹腔注射剂量为3-30 mg / kg的Ciclazindol会增加VO2，但似乎不会增加运动活性或引起CNS刺激的任何其他迹象，包括延长入睡时间或定型观念。仅在使用最低剂量的mazindol（0.3 mg / kg i.p.）时才发生代谢和CNS作用的分离。这些结果可能反映了（a）这些药物抑制大脑和棕色脂肪去甲肾上腺素摄取过程的相对能力，以及（b）ciclazindol在棕色脂肪中相对较高的积累。 4在所测试的药物中，棕色皮肤脂肪组织（BAT）中仅ciclazindol对去甲肾上腺素摄取系统的抑制作用强于大脑。动力学分析还表明，ciclazindol对BAT中的NA吸收系统和Na +，K + -ATPase的作用不同于mazindol。 5这些发现表明，ciclazindol可能在啮齿动物中产生能量消耗效应，而不会引起明显的CNS刺激。讨论了这些发现对人类肥胖的影响。

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