Is There Appetite after GLP‐1 and PACAP?
Is There Appetite after GLP‐1 and PACAP?
复制标题
GLP-1 和 PACAP 后有食欲吗？
DOI：
10.1111/j.1749-6632.1998.tb11192.x
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发表时间：
1998
影响因子：
5.2
通讯作者：
Jean Christophe
中科院分区：
文献类型：
--
作者：
Jean Christophe
摘要：抗肥胖药物必须增加下丘脑饱腹感中枢对瘦素的敏感性，并拮抗NPY的合成和作用。现有的药理学工具种类繁多，但目前效果不佳。在考虑评估的肽类似物[NPY‐5拮抗剂和CCK‐A， bombesin， amylin和黑色素细胞刺激激素- 4（或黑色素浓缩激素？）激动剂]中，GLP‐1和PACAP是否有一席之地？GLP‐1受体存在于ARC、PVN、VMN和SON中，是具有GLUT‐2和葡萄糖激酶的下丘脑神经元中枢性和血源性GLP‐1的靶标。GLP‐1是一种有效的胰岛素促胰岛素剂，由L‐细胞在餐后高分泌，与葡萄糖一起减少食物摄入并诱导ARC中的c‐fos。PACAP存在于ARC、PVN和SCH中，其下丘脑I型受体升高PVN中的cAMP和三磷酸肌醇，在那里它可能对抗NPY诱导的食物摄入和高胰岛素血症。然而，不相关的神经内分泌、自主神经和昼夜节律功能也被这种肽激活，使其成为建立肥胖治疗的不理想基础。
Abstract: Anitobesity drugs must increase the sensitivity of the hypothalamic satiety center towards leptin and antagonize the synthesis and action of NPY. The array of pharmacologic tools available is vast and presently ineffective. Among peptide analogs considered for evaluation [NPY‐5 antagonists and CCK‐A, bombesin, amylin and melanocyte‐stimulating hormone‐4 (or melanin‐concentrating hormone?) agonists], is there a place for GLP‐1 and PACAP? GLP‐1 receptors present in ARC, PVN, VMN, and SON are the target for both central and blood‐borne GLP‐1 in those hypothalamic neurons endowed with GLUT‐2 and glucokinase. GLP‐1, hypersecreted by L‐cells after a meal, is a potent insulinotropic agent and, together with glucose, reduces food intake and induces c‐fos in the ARC. PACAP is present in the ARC, PVN, and SCH, and its hypothalamic type I receptor elevates cAMP and inositol triphosphate in the PVN, where it may perhaps antagonize NPY‐induced food intake and hyperinsulinemia. However, irrelevant neuroendocrine, autonomic, and circadian functions are also activated by this peptide, making it a less than ideal base on which to build an obesity treatment.
影响因子：
4.8
作者：
M. Schwartz;A. Sipols;J. L. Marks;G. Sanacora;Jeffery D. White;A. Scheurink;S. Kahn;D. Baskin;S. Woods;D. Figlewicz
通讯作者：
M. Schwartz;A. Sipols;J. L. Marks;G. Sanacora;Jeffery D. White;A. Scheurink;S. Kahn;D. Baskin;S. Woods;D. Figlewicz
使用和不使用胰岛素替代治疗的链脲佐菌素糖尿病大鼠的显微解剖下丘脑区域中的神经肽-Y 浓度以及下丘脑内侧基底视前区的体外释放。
影响因子：
4.8
作者：
Sahu,A;Sninsky,CA;Kalra,PS;Kalra,SP
通讯作者：
Kalra,SP
影响因子：
3.6
作者：
Sheriff, S;Chance, WT;Balasubramaniam, A
通讯作者：
Balasubramaniam, A