• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

关于胆囊收缩素(CCK)在调节小鼠食物摄入量方面生理作用的证据。

Evidence for a physiological role for CCK in the regulation of food intake in mice.

作者信息

Silver A J, Flood J F, Song A M, Morley J E

机构信息

Geriatric Research, Education, and Clinical Center, Sepulveda Veterans Administration Medical Center 91343.

出版信息

Am J Physiol. 1989 Mar;256(3 Pt 2):R646-52. doi: 10.1152/ajpregu.1989.256.3.R646.

DOI:10.1152/ajpregu.1989.256.3.R646
PMID:2923253
Abstract

The effects of L-364,718, a cholecystokinin receptor antagonist, on cholecystokinin octapeptide-induced inhibition of food, and its effect on food intake when given alone, were studied in mice using several different feeding paradigms. In all studies, L-364,718 (100 micrograms/kg, 1.0 mg/kg) reversed the ability of cholecystokinin octapeptide to decrease food intake. L-364,718 enhanced food consumption compared with controls in nonfasted mice (100 microgram/kg) and in prefed mice (50, 100, 250 micrograms/kg). The number of reinforcements, using a lever press, was also enhanced by L-364,718 (100 micrograms/kg) compared with control. In other paradigms, L-364,718 failed to enhance food intake. These results are compatible with the suggestion that cholecystokinin may play a physiological role in the regulation of food intake.

摘要

在小鼠中,使用几种不同的进食模式,研究了胆囊收缩素受体拮抗剂L-364,718对胆囊收缩素八肽诱导的进食抑制的影响,以及单独给药时对食物摄入量的影响。在所有研究中,L-364,718(100微克/千克、1.0毫克/千克)逆转了胆囊收缩素八肽减少食物摄入量的能力。与未禁食小鼠(100微克/千克)和预喂小鼠(50、100、250微克/千克)中的对照组相比,L-364,718增加了食物消耗量。与对照组相比,L-364,718(100微克/千克)通过杠杆按压增加的强化次数也更多。在其他模式中,L-364,718未能增加食物摄入量。这些结果与胆囊收缩素可能在食物摄入调节中发挥生理作用的观点一致。

相似文献

1
Evidence for a physiological role for CCK in the regulation of food intake in mice.关于胆囊收缩素(CCK)在调节小鼠食物摄入量方面生理作用的证据。
Am J Physiol. 1989 Mar;256(3 Pt 2):R646-52. doi: 10.1152/ajpregu.1989.256.3.R646.
2
Potent cholecystokinin antagonist L 364718 stimulates food intake in rats.强效胆囊收缩素拮抗剂L 364718刺激大鼠进食。
Am J Physiol. 1989 Dec;257(6 Pt 2):R1512-8. doi: 10.1152/ajpregu.1989.257.6.R1512.
3
Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice.瘦素与胆囊收缩素之间的协同相互作用可减少瘦小鼠的短期食物摄入量。
Proc Natl Acad Sci U S A. 1997 Sep 16;94(19):10455-60. doi: 10.1073/pnas.94.19.10455.
4
Satiety induced by endogenous and exogenous cholecystokinin is mediated by CCK-A receptors in mice.内源性和外源性胆囊收缩素诱导的饱腹感是由小鼠体内的CCK-A受体介导的。
Am J Physiol. 1992 Apr;262(4 Pt 2):R574-8. doi: 10.1152/ajpregu.1992.262.4.R574.
5
Use of a specific cholecystokinin receptor antagonist (L-364,718) to determine the role of cholecystokinin on feeding and body weight in rats with obstructive jaundice.
J Assoc Acad Minor Phys. 1992;3(2):38-40.
6
Fluoxetine reduces food intake by a cholecystokinin-independent mechanism.氟西汀通过一种不依赖胆囊收缩素的机制减少食物摄入量。
Pharmacol Biochem Behav. 1990 Jan;35(1):51-4. doi: 10.1016/0091-3057(90)90203-t.
7
Devazepide alters meal patterns in lean, but not obese, male Zucker rats.地伐西匹改变了瘦型雄性 Zucker 大鼠的进食模式,但对肥胖型雄性 Zucker 大鼠无效。
Physiol Behav. 1994 Nov;56(5):1037-9. doi: 10.1016/0031-9384(94)90340-9.
8
Type-A CCK receptors mediate the inhibition of food intake and activity by CCK-8 in 9- to 12-day-old rat pups.A型胆囊收缩素受体介导胆囊收缩素-8对9至12日龄幼鼠食物摄入和活动的抑制作用。
Pharmacol Biochem Behav. 1991 Jan;38(1):207-10. doi: 10.1016/0091-3057(91)90612-6.
9
The cholecystokinin receptor antagonist L364,718 increases food intake in the rat by attenuation of the action of endogenous cholecystokinin.胆囊收缩素受体拮抗剂L364,718通过减弱内源性胆囊收缩素的作用来增加大鼠的食物摄入量。
Br J Pharmacol. 1988 Jan;93(1):79-84. doi: 10.1111/j.1476-5381.1988.tb11407.x.
10
Effects of the CCK receptor antagonist MK-329 on food intake in pigs.胆囊收缩素受体拮抗剂MK-329对猪采食量的影响。
Physiol Behav. 1990 Jan;47(1):145-8. doi: 10.1016/0031-9384(90)90053-7.

引用本文的文献

1
Stress integration by an ascending adrenergic-melanocortin circuit.通过一条上行肾上腺素能-促黑素细胞激素回路进行应激整合。
Neuropsychopharmacology. 2024 Aug;49(9):1361-1372. doi: 10.1038/s41386-024-01810-9. Epub 2024 Feb 7.
2
Satietogenic Protein from Tamarind Seeds Decreases Food Intake, Leptin Plasma and CCK-1r Gene Expression in Obese Wistar Rats.罗望子种子中的饱腹蛋白可降低肥胖 Wistar 大鼠的食物摄入量、血浆瘦素和 CCK-1r 基因表达。
Obes Facts. 2018;11(6):440-453. doi: 10.1159/000492733. Epub 2018 Dec 11.
3
Anorexia of ageing: a key component in the pathogenesis of both sarcopenia and cachexia.
衰老性厌食:肌肉减少症和恶病质发病机制中的关键组成部分。
J Cachexia Sarcopenia Muscle. 2017 Aug;8(4):523-526. doi: 10.1002/jcsm.12192. Epub 2017 Apr 27.
4
Dissecting carboxypeptidase E: properties, functions and pathophysiological roles in disease.剖析羧肽酶E:疾病中的特性、功能及病理生理作用
Endocr Connect. 2017 May;6(4):R18-R38. doi: 10.1530/EC-17-0020. Epub 2017 Mar 27.
5
Pathophysiology of anorexia in the cancer cachexia syndrome.癌症恶病质综合征中厌食的病理生理学
J Cachexia Sarcopenia Muscle. 2015 Dec;6(4):287-302. doi: 10.1002/jcsm.12059. Epub 2015 Oct 27.
6
Gut vagal afferents are necessary for the eating-suppressive effect of intraperitoneally administered ginsenoside Rb1 in rats.内脏迷走传入神经对于腹腔注射人参皂苷Rb1对大鼠进食的抑制作用是必需的。
Physiol Behav. 2015 Dec 1;152(Pt A):62-7. doi: 10.1016/j.physbeh.2015.09.012. Epub 2015 Sep 15.
7
Vagal control of satiety and hormonal regulation of appetite.迷走神经对饱腹感的控制和激素对食欲的调节。
J Neurogastroenterol Motil. 2011 Oct;17(4):338-48. doi: 10.5056/jnm.2011.17.4.338. Epub 2011 Oct 31.
8
Characterization of the feeding inhibition and neural activation produced by dorsomedial hypothalamic cholecystokinin administration.下丘脑背内侧注射胆囊收缩素所产生的摄食抑制和神经激活的特征
Neuroscience. 2008 Mar 3;152(1):178-88. doi: 10.1016/j.neuroscience.2007.12.004.
9
Neuronal control of energy homeostasis.能量稳态的神经元控制。
FEBS Lett. 2008 Jan 9;582(1):132-41. doi: 10.1016/j.febslet.2007.11.063. Epub 2007 Dec 3.
10
Hyperphagia and obesity in OLETF rats lacking CCK-1 receptors.缺乏胆囊收缩素-1受体的OLETF大鼠出现食欲亢进和肥胖。
Philos Trans R Soc Lond B Biol Sci. 2006 Jul 29;361(1471):1211-8. doi: 10.1098/rstb.2006.1857.