Capsaicin abolishes lipoprivic but not glucoprivic feeding in rats.
Capsaicin abolishes lipoprivic but not glucoprivic feeding in rats.
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辣椒素可以消除大鼠的禁脂喂养，但不能取消禁糖喂养。
DOI：
10.1152/ajpregu.1989.256.6.r1232
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Taylor,JS
中科院分区：
文献类型：
--
作者：
Ritter,S;Taylor,JS
为了评估内脏感觉神经元对葡萄糖和脂肪酸代谢阻断诱导的进食的贡献，将成年大鼠麻醉并用辣椒素进行全身治疗，辣椒素是一种破坏细直径无髓鞘初级感觉神经元（包括许多内脏感觉神经元）的毒素。在整个实验过程中，大鼠均维持补充脂肪的饮食。对于喂养试验，分别用巯基乙酸酯（MA）或2-脱氧-D-葡萄糖（2-DG）全身阻断脂肪酸或葡萄糖利用后，在同时施用MA和2-DG后以及注射盐水后，每小时测量该饮食的摄入量，持续6小时。 2-DG 刺激剂量相关的进食反应，在辣椒素和媒介物处理的大鼠中，其幅度相似。 MA 还刺激了媒介物治疗大鼠的剂量相关的进食反应。然而，接受辣椒素处理的大鼠并没有对 MA 做出反应而进食。此外，2-DG和MA在媒介物处理的对照中对摄食的刺激是相加的，但辣椒素处理的大鼠在2-DG加MA后的进食量与仅对2-DG的反应相同。因此，葡萄糖缺乏和脂肪缺乏激活了解剖学和化学上不同的受体，以控制进食的代谢。
To assess the contribution of visceral sensory neurons to feeding induced by blockade of glucose and fatty acid metabolism, adult rats were anesthetized and treated systemically with capsaicin, a toxin that destroys fine-diameter unmyelinated primary sensory neurons, including many visceral sensory neurons. Rats were maintained on a fat-supplemented diet throughout experimentation. For feeding tests, intake of this diet was measured hourly for 6 h after systemic blockade of fatty acid or glucose utilization with mercaptoacetate (MA) or 2-deoxy-D-glucose (2-DG), respectively, after simultaneous administration of MA and 2-DG and after saline injection. 2-DG stimulated a dose-related feeding response that was similar in magnitude in both capsaicin and vehicle-treated rats. MA also stimulated a dose-related feeding response in vehicle-treated rats. However, capsaicin-treated rats did not eat in response to MA. In addition, 2-DG and MA were additive in their stimulation of feeding in vehicle-treated controls, but capsaicin-treated rats ate the same amount after 2-DG plus MA as they did in response to 2-DG alone. Thus glucoprivation and lipoprivation activate anatomically and chemically distinct receptors for the metabolic control of feeding.