Endogenous amylin contributes to the anorectic effects of cholecystokinin and bombesin
Endogenous amylin contributes to the anorectic effects of cholecystokinin and bombesin
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DOI：
10.1016/s0196-9781(02)00280-2
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发表时间：
2003-01-01
期刊：
影响因子：
3
通讯作者：
Lutz, TA
中科院分区：
文献类型：
--
作者：
Mollet, A;Meier, S;Lutz, TA
胰淀素可能通过促进胰淀素的释放或调节其在中枢神经系统（CNS）内的减食欲作用而参与胆囊收缩素（CCK）和蛙皮素（BBS）的减食欲作用。我们研究了腹腔注射CCK或BBS对淀粉样蛋白缺陷小鼠（IAPP（-/-））进食的影响。与野生型（WT）小鼠相比，CCK和BBS在IAPP-/-小鼠中的厌食作用几乎被消除（如20 μ g/kg CCK，1小时摄食量：WT/NaCl 0.53 ± 0.03 g，WT/CCK 0.16 ± 0.03 g（P < 0.001），IAPP（-/-）/NaCl 0.49 ± 0.05 g，IAPP（-/-）/CCK 0.39 +/- 0.04 g）。急性胰淀素替代恢复了CCK对IAPP-/小鼠的厌食作用。为了发现CCK或BBS是否增强了喂养诱导的胰腺胰淀素的释放，我们给大鼠注射CCK-8（0.5-50 μ g/kg）或BBS（5 μ g/kg），并在注射后测量血浆胰淀素水平。CCK和BBS均不增加大鼠血浆胰淀素水平。我们认为胰淀素对CCK和BBS的厌食作用的调节不依赖于CCK或BBS诱导的胰淀素释放，而可能是由于胰淀素在CNS内调节其作用。(C)2002年爱思唯尔科技有限公司All rights reserved.
Previous studies indicated that amylin contributes to the anorectic effects of cholecystokinin (CCK) and bombesin (BBS), possibly by enhancing the release of pancreatic amylin or by modulating their anorectic actions within the central nervous system (CNS).To elucidate the interaction between amylin and CCK or BBS, respectively, we investigated the influence of an IP injection of CCK or BBS on feeding in amylin-deficient mice (IAPP(-/-)). The anorectic effects of CCK and BBS were nearly abolished in IAPP-/- mice compared to wildtype (WT) mice (e.g. 20 mug/kg CCK, 1-h food intake: WT/NaCl 0.53 +/- 0.03 g; WT/CCK 0.16 +/- 0.03 g (P < 0.001); IAPP(-/-)/NaCl 0.49 +/- 0.05 g; IAPP(-/-)/CCK 0.39 +/- 0.04 g). Acute amylin replacement restored the anorectic effect of CCK in IAPP-/mice.To find out whether CCK or BBS enhance the feeding-induced release of pancreatic amylin, we injected rats with CCK-8 (0.5-50 mu g/kg) or BBS (5 mu g/kg) and measured plasma amylin levels after injections. Neither CCK nor BBS increased the plasma amylin level in rats. We suggest that the mediation of the anorectic effects of CCK and BBS by amylin is not dependent on a CCK- or BBS-induced release of pancreatic amylin, but may rather be due to a modulation of their effects by amylin within the CNS. (C) 2002 Elsevier Science Inc. All rights reserved.