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辣椒素可消除大鼠的脂肪缺乏性进食,但不能消除葡萄糖缺乏性进食。

Capsaicin abolishes lipoprivic but not glucoprivic feeding in rats.

作者信息

Ritter S, Taylor J S

机构信息

Department of Veterinary and Comparative Anatomy, Washington State University, Pullman 99164-6520.

出版信息

Am J Physiol. 1989 Jun;256(6 Pt 2):R1232-9. doi: 10.1152/ajpregu.1989.256.6.R1232.

DOI:10.1152/ajpregu.1989.256.6.R1232
PMID:2735449
Abstract

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.

摘要

为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作用,成年大鼠被麻醉并全身注射辣椒素,辣椒素是一种毒素,可破坏细直径无髓初级感觉神经元,包括许多内脏感觉神经元。在整个实验过程中,大鼠维持高脂饮食。对于进食测试,在用巯基乙酸盐(MA)或2-脱氧-D-葡萄糖(2-DG)分别全身阻断脂肪酸或葡萄糖利用后、同时给予MA和2-DG后以及注射生理盐水后,每小时测量6小时内这种饮食的摄入量。2-DG刺激了剂量相关的进食反应,在辣椒素处理组和对照组大鼠中反应强度相似。MA也在对照组大鼠中刺激了剂量相关的进食反应。然而,辣椒素处理组大鼠对MA无进食反应。此外,在对照组中,2-DG和MA对进食的刺激作用具有相加性,但辣椒素处理组大鼠在2-DG加MA后进食量与单独给予2-DG时相同。因此,糖剥夺和脂剥夺通过解剖学和化学上不同的受体来激活对进食的代谢控制。

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