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可卡因和苯丙胺调节转录肽（CART）与胆囊收缩素对瘦小鼠食物摄入调节的协同作用。

Synergistic effect of CART (cocaine- and amphetamine-regulated transcript) peptide and cholecystokinin on food intake regulation in lean mice.

作者信息

Maletínská Lenka, Maixnerová Jana, Matysková Resha, Haugvicová Renata, Pirník Zdeno, Kiss Alexander, Zelezná Blanka

机构信息

Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, Flemingovo nám, 2, 16610 Prague 6, Czech Republic.

出版信息

BMC Neurosci. 2008 Oct 21;9:101. doi: 10.1186/1471-2202-9-101.

DOI:10.1186/1471-2202-9-101
PMID:18939974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2587474/
Abstract

BACKGROUND

CART (cocaine- and amphetamine-regulated transcript) peptide and cholecystokinin (CCK) are neuromodulators involved in feeding behavior. This study is based on previously found synergistic effect of leptin and CCK on food intake and our hypothesis on a co-operation of the CART peptide and CCK in food intake regulation and Fos activation in their common targets, the nucleus tractus solitarii of the brainstem (NTS), the paraventricular nucleus (PVN), and the dorsomedial nucleus (DMH) of the hypothalamus.

RESULTS

In fasted C57BL/6 mice, the anorexigenic effect of CART(61-102) in the doses of 0.1 or 0.5 microg/mouse was significantly enhanced by low doses of CCK-8 of 0.4 or 4 microg/kg, while 1 mg/kg dose of CCK-A receptor antagonist devazepide blocked the effect of CART(61-102) on food intake. After simultaneous administration of 0.1 microg/mouse CART(61-102) and of 4 microg/kg of CCK-8, the number of Fos-positive neurons in NTS, PVN, and DMH was significantly higher than after administration of each particular peptide. Besides, CART(61-102) and CCK-8 showed an additive effect on inhibition of the locomotor activity of mice in an open field test.

CONCLUSION

The synergistic and long-lasting effect of the CART peptide and CCK on food intake and their additive effect on Fos immunoreactivity in their common targets suggest a co-operative action of CART peptide and CCK which could be related to synergistic effect of leptin on CCK satiety.

摘要

背景

可卡因和苯丙胺调节转录肽（CART）和胆囊收缩素（CCK）是参与进食行为的神经调质。本研究基于先前发现的瘦素和CCK对食物摄入的协同作用，以及我们关于CART肽和CCK在食物摄入调节以及它们共同靶点——脑干孤束核（NTS）、下丘脑室旁核（PVN）和背内侧核（DMH）中的Fos激活方面存在合作的假设。

结果

在禁食的C57BL/6小鼠中，0.4或4微克/千克的低剂量CCK-8可显著增强0.1或0.5微克/只剂量的CART(61 - 102)的厌食作用，而1毫克/千克剂量的CCK-A受体拮抗剂地伐西匹可阻断CART(61 - 102)对食物摄入的影响。同时给予0.1微克/只的CART(61 - 102)和4微克/千克的CCK-8后，NTS、PVN和DMH中Fos阳性神经元的数量显著高于单独给予每种肽后的数量。此外，在旷场试验中，CART(61 - 102)和CCK-8对小鼠运动活动的抑制表现出相加作用。

结论

CART肽和CCK对食物摄入的协同和持久作用以及它们在共同靶点上对Fos免疫反应性的相加作用表明，CART肽和CCK存在合作作用，这可能与瘦素对CCK饱腹感的协同作用有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07b4/2587474/ea6d06f298fc/1471-2202-9-101-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07b4/2587474/4ae4d4e12383/1471-2202-9-101-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07b4/2587474/e17b39ce3588/1471-2202-9-101-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07b4/2587474/cb4c62670e16/1471-2202-9-101-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07b4/2587474/ea6d06f298fc/1471-2202-9-101-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07b4/2587474/4ae4d4e12383/1471-2202-9-101-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07b4/2587474/e17b39ce3588/1471-2202-9-101-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07b4/2587474/cb4c62670e16/1471-2202-9-101-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07b4/2587474/ea6d06f298fc/1471-2202-9-101-4.jpg

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