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果蝇中的抗肥胖神经元。

Obesity-blocking neurons in Drosophila.

作者信息

Al-Anzi Bader, Sapin Viveca, Waters Christopher, Zinn Kai, Wyman Robert J, Benzer Seymour

机构信息

Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.

出版信息

Neuron. 2009 Aug 13;63(3):329-41. doi: 10.1016/j.neuron.2009.07.021.

DOI:10.1016/j.neuron.2009.07.021
PMID:19679073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2742587/
Abstract

In mammals, fat store levels are communicated by leptin and insulin signaling to brain centers that regulate food intake and metabolism. By using transgenic manipulation of neural activity, we report the isolation of two distinct neuronal populations in flies that perform a similar function, the c673a-Gal4 and fruitless-Gal4 neurons. When either of these neuronal groups is silenced, fat store levels increase. This change is mediated through an increase in food intake and altered metabolism in c673a-Gal4-silenced flies, while silencing fruitless-Gal4 neurons alters only metabolism. Hyperactivation of either neuronal group causes depletion of fat stores by increasing metabolic rate and decreasing fatty acid synthesis. Altering the activities of these neurons causes changes in expression of genes known to regulate fat utilization. Our results show that the fly brain measures fat store levels and can induce changes in food intake and metabolism to maintain them within normal limits.

摘要

在哺乳动物中,脂肪储存水平通过瘦素和胰岛素信号传递至调节食物摄入和新陈代谢的脑区。通过对神经活动进行转基因操作,我们报告在果蝇中分离出了两个执行类似功能的不同神经元群体,即c673a - Gal4神经元和无果 - Gal4神经元。当沉默这些神经元群体中的任何一个时,脂肪储存水平会升高。这种变化在c673a - Gal4沉默的果蝇中是通过食物摄入量增加和新陈代谢改变介导的,而沉默无果 - Gal4神经元仅改变新陈代谢。任一神经元群体的过度激活会通过提高代谢率和减少脂肪酸合成导致脂肪储存耗尽。改变这些神经元的活动会导致已知调节脂肪利用的基因表达发生变化。我们的结果表明,果蝇大脑能够测量脂肪储存水平,并可诱导食物摄入和新陈代谢的变化,以将其维持在正常范围内。

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