A role for pancreatic polypeptide in feeding and body weight regulation

A role for pancreatic polypeptide in feeding and body weight regulation
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DOI:
10.1016/j.peptides.2006.09.024
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发表时间:
2007-02-01
期刊:
影响因子:
3
通讯作者:
Inui, Akio
Inui, Akio
中科院分区:
医学3区
文献类型:
--
作者:
Kojima, Shinya;Ueno, Naohiko;Inui, Akio

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PP 给药通过抑制食物摄入和胃排空同时增加啮齿动物的能量消耗来诱导负能量平衡。 PP的作用机制涉及下丘脑摄食调节肽表达的变化以及迷走神经-迷走神经和迷走神经-交感神经反射弧的活动。我们开发的 PP 过表达小鼠表现出瘦弱表型,食物摄入量和胃排空率降低。转基因小鼠血浆胆囊收缩素(CCK)浓度增加,CCK-1受体拮抗剂改善了动物的厌食症。这些结果,与先前关于 PP 作为胰腺外分泌分泌和胆囊收缩中的抗 CCK 激素的概念一起,表明 PP-CCK 相互作用可能是拮抗的或协同的,并且转基因小鼠可能因 PP 和 CCK 的过量产生而表现出混合表型。 (c) 2006 Elsevier Inc. 保留所有权利。
PP administration induces negative energy balance by suppressing food intake and gastric emptying while increasing energy expenditure in rodents. The mechanism of PP actions involves the changes in the expression of hypothalamic feeding-regulatory peptides and the activity of the vago-vagal and vago-sympathetic reflex arc. PP-overexpressing mice we developed exhibited the thin phenotype with decreased food intake and gastric emptying rate. Plasma cholecystokinin (CCK) concentrations were increased in the transgenic mice and CCK-1 receptor antagonist improved the anorexia of the animals. These results, together with the previous notion of PP as an anti-CCK hormone in pancreatic exocrine secretion and gallbladder contraction, indicate that PP-CCK interactions may be either antagonistic or synergistic and the transgenic mice may exhibit the mixed phenotype by overproduction of PP and CCK. (c) 2006 Elsevier Inc. All rights reserved.