Goldstone A P, Morgan I, Mercer J G, Morgan D G, Moar K M, Ghatei M A, Bloom S R
Endocrine Unit, Hammersmith Hospital, London, W12 0NN, United Kingdom.
Biochem Biophys Res Commun. 2000 Mar 16;269(2):331-5. doi: 10.1006/bbrc.2000.2288.
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 post-translational 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 expression 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.
瘦素，这种由脂肪细胞产生的血浆激素，以及中枢神经系统（CNS）中的胰高血糖素样肽-1（GLP-1）神经元可减少食物摄入量和体重。GLP-1是由前胰高血糖素原经翻译后加工在中枢神经系统中产生的。脑室内注射瘦素可防止成对喂养饮食受限大鼠下丘脑GLP-1肽含量的降低（P<0.05）。孤束核（NTS）中前胰高血糖素原mRNA表达与下丘脑GLP-1肽含量之间存在显著的总体正相关（r=+0.34，P<0.05）。腹腔注射瘦素也可增加饮食受限小鼠下丘脑GLP-1肽含量（P<0.05）。这支持了瘦素的厌食作用部分归因于对GLP-1神经元的刺激这一假说。食物剥夺期间中枢神经系统GLP-1神经元活性降低可能会刺激进食行为，或许还会抑制下丘脑促性腺激素释放激素（LHRH）神经元，作为对饥饿的神经内分泌反应的一部分。
