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A cholecystokinin-1 receptor agonist (CCK-8) mediates increased permeability of brain barriers to leptin

机译:胆囊收缩素-1受体激动剂(CCK-8)介导脑屏障对瘦素的通透性增加

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摘要

Background and purpose:Leptin regulates energy expenditure and body weight by acting both on the hypothalamus and on peripheral targets. Central actions of leptin are enhanced by cholecystokinin (CCK). The interaction between leptin and CCK makes physiological sense, as rats lacking CCK1 receptors are resistant to peripheral leptin but not to leptin directly infused into the brain. We have recently reported that CCK enhances leptin effects by increasing the entry of leptin into the CNS. The aim of this work was to further characterize the effect of CCK (10 μg kg−1) on leptin kinetics as well as the CCK receptor subtype involved in the interaction between CCK and leptin.
机译:背景和目的:瘦素通过作用于下丘脑和周围靶标来调节能量消耗和体重。胆囊收缩素(CCK)可增强瘦素的中枢作用。瘦素与CCK之间的相互作用具有生理意义,因为缺乏CCK1受体的大鼠对周围的瘦素具有抵抗力,但对直接注入大脑的瘦素没有抵抗力。我们最近报道,CCK通过增加瘦素进入中枢神经系统来增强瘦素作用。这项工作的目的是进一步表征CCK(10μggkgkg -1 )对瘦素动力学以及参与CCK和瘦素相互作用的CCK受体亚型的影响。

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