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本文引用的文献

1
Obestatin inhibits motor activity in the antrum and duodenum in the fed state of conscious rats.肥胖抑制素在清醒大鼠进食状态下抑制胃窦和十二指肠的运动活性。
Am J Physiol Gastrointest Liver Physiol. 2008 May;294(5):G1210-8. doi: 10.1152/ajpgi.00549.2007. Epub 2008 Mar 6.
2
Obestatin reduces food intake and suppresses body weight gain in rodents.肥胖抑制素可减少啮齿动物的食物摄入量并抑制体重增加。
Biochem Biophys Res Commun. 2007 May 25;357(1):264-9. doi: 10.1016/j.bbrc.2007.03.138. Epub 2007 Mar 30.
3
Effect of peripheral obestatin on gastric emptying and intestinal contractility in rodents.外周肥胖抑制素对啮齿动物胃排空和肠收缩性的影响。
Neurogastroenterol Motil. 2007 Mar;19(3):211-7. doi: 10.1111/j.1365-2982.2006.00883.x.
4
Comment on "Obestatin, a peptide encoded by the ghrelin gene, opposes ghrelin's effects on food intake".对“胃饥饿素基因编码的一种肽——肥胖抑制素,对抗胃饥饿素对食物摄入的影响”的评论
Science. 2007 Feb 9;315(5813):766; author reply 766. doi: 10.1126/science.1135047.
5
Little or no ability of obestatin to interact with ghrelin or modify motility in the rat gastrointestinal tract.胃饥饿素在大鼠胃肠道中与胃促生长素相互作用或改变运动的能力很小或没有。
Br J Pharmacol. 2007 Jan;150(1):58-64. doi: 10.1038/sj.bjp.0706969. Epub 2006 Nov 27.
6
Normal food intake and body weight in mice lacking the G protein-coupled receptor GPR39.缺乏G蛋白偶联受体GPR39的小鼠的正常食物摄入量和体重
Endocrinology. 2007 Feb;148(2):501-6. doi: 10.1210/en.2006-1275. Epub 2006 Nov 9.
7
Obestatin inhibits feeding but does not modulate GH and corticosterone secretion in the rat.肥胖抑制素可抑制大鼠进食,但不调节其生长激素和皮质酮的分泌。
J Endocrinol Invest. 2006 Sep;29(8):RC16-8. doi: 10.1007/BF03344175.
8
Effects of obestatin on energy balance and growth hormone secretion in rodents.肥胖抑制素对啮齿动物能量平衡及生长激素分泌的影响。
Endocrinology. 2007 Jan;148(1):21-6. doi: 10.1210/en.2006-0915. Epub 2006 Sep 28.
9
GPR39 signaling is stimulated by zinc ions but not by obestatin.GPR39信号传导由锌离子刺激,而非由肥胖抑制素刺激。
Endocrinology. 2007 Jan;148(1):13-20. doi: 10.1210/en.2006-0933. Epub 2006 Sep 7.
10
Lack of interaction between peripheral injection of CCK and obestatin in the regulation of gastric satiety signaling in rodents.外周注射胆囊收缩素(CCK)与肥胖抑制素在调节啮齿动物胃饱腹感信号方面缺乏相互作用。
Peptides. 2006 Nov;27(11):2811-9. doi: 10.1016/j.peptides.2006.07.012. Epub 2006 Aug 24.

胃饥饿素、去酰基胃饥饿素和肥胖抑制素对清醒大鼠胃十二指肠运动的不同影响。

Different effects of ghrelin, des-acyl ghrelin and obestatin on gastroduodenal motility in conscious rats.

作者信息

Fujimiya Mineko, Asakawa Akihiro, Ataka Koji, Kato Ikuo, Inui Akio

机构信息

Department of Anatomy, Sapporo Medical University, School of Medicine, Chuo-ku, Sapporo 060-8556, Japan.

出版信息

World J Gastroenterol. 2008 Nov 7;14(41):6318-26. doi: 10.3748/wjg.14.6318.

DOI:10.3748/wjg.14.6318
PMID:19009646
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2766112/
Abstract

Three peptides, ghrelin, des-acyl ghrelin and obestatin are derived from a common prohormone, preproghrelin by posttranslational processing, originating from endocrine cells in the stomach. To examine the effects of these peptides, we applied the manometric measurement of gastrointestinal motility in freely moving conscious rat models. Ghrelin exerts stimulatory effects on the motility of antrum and duodenum in both fed and fasted state of animals. Des-acyl ghrelin exerts inhibitory effects on the motility of antrum, but not on the motility of duodenum in the fasted state of animals. Obestatin exerts inhibitory effects on the motility of antrum and duodenum in the fed state, but not in the fasted state of animals. NPY Y2 or Y4 receptors in the brain may mediate the action of ghrelin, CRF type 2 receptors in the brain mediate the action of des-acyl ghrelin, whereas CRF type 1 and type 2 receptors in the brain mediate the action of obestatin. Vagal afferent pathways might be involved in the action of ghrelin, but not involved in the action of des-acyl ghrelin, whereas vagal afferent pathways might be partially involved in the action of obestatin.

摘要

三种肽,即胃饥饿素、去酰基胃饥饿素和肥胖抑制素,是由一种共同的前激素——前胃饥饿素原经翻译后加工产生的,它们源自胃中的内分泌细胞。为了研究这些肽的作用,我们在自由活动的清醒大鼠模型中应用了胃肠动力的压力测量法。胃饥饿素在动物的进食和禁食状态下均对胃窦和十二指肠的动力产生刺激作用。去酰基胃饥饿素在动物禁食状态下对胃窦动力产生抑制作用,但对十二指肠动力无抑制作用。肥胖抑制素在动物进食状态下对胃窦和十二指肠动力产生抑制作用,但在禁食状态下无此作用。大脑中的神经肽Y Y2或Y4受体可能介导胃饥饿素的作用,大脑中的促肾上腺皮质激素释放因子2型受体介导去酰基胃饥饿素的作用,而大脑中的促肾上腺皮质激素释放因子1型和2型受体介导肥胖抑制素的作用。迷走神经传入通路可能参与胃饥饿素的作用,但不参与去酰基胃饥饿素的作用,而迷走神经传入通路可能部分参与肥胖抑制素的作用。