Effect of leptin on hypothalamic GLP-1 peptide and brain-stem pre-proglucagon mRNA
Effect of leptin on hypothalamic GLP-1 peptide and brain-stem pre-proglucagon mRNA
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DOI：
10.1006/bbrc.2000.2288
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发表时间：
2000-03-16
影响因子：
3.1
通讯作者：
Bloom, SR
中科院分区：
文献类型：
--
作者：
Goldstone, AP;Morgan, I;Bloom, SR
瘦素（脂肪细胞来源的血浆激素）和CNS GLP-1神经元减少食物摄入和体重。GLP-1在CNS中通过前胰高血糖素原的翻译后加工产生。ICV给予瘦素可防止成对喂养的食物限制大鼠下丘脑GLP-1肽含量的降低（P < 0.05）。NTS前胰高血糖素原mRNA表达与下丘脑GLP-1肽含量呈显著正相关（r =+0.34，P < 0.05）。腹腔注射瘦素也能增加限食小鼠下丘脑GLP-1肽的含量（P < 0.05）。这支持了瘦素的厌食作用部分是由于GLP-1神经元的刺激的假设。在食物剥夺期间降低的CNS GLP-1神经元活性可能起到刺激进食行为的作用，并且可能还抑制下丘脑LHRH神经元，作为对饥饿的神经内分泌反应的一部分。(C)北京大学出版社.
Leptin, the adipocyte-derived plasma hormone, and CNS GLP-1 neurons reduce food intake and body weight. GLP-1 is produced in the CNS by posttranslational processing of pre-proglucagon. ICV leptin administration prevented the reduction in hypothalamic GLP-1 peptide content seen in pair-fed food-restricted rats (P < 0.05). There was a significant overall positive correlation between pre-proglucagon mRNA expreession in the NTS and hypothalamic GLP-1 peptide content (r = +0.34, P < 0.05). Intraperitoneal leptin administration also increased hypothalamic GLP-1 peptide in food-restricted mice (P < 0.05). This supports the hypothesis that the anorectic actions of leptin are in part due to stimulation of GLP-1 neurons. Reduced CNS GLP-1 neuronal; activity during food deprivation may act to stimulate feeding behaviour, and perhaps also inhibit hypothalamic LHRH neurons, as part of the neuroendocrine response to starvation. (C) 2000 Academic Press.