Obesity-Blocking Neurons in Drosophila

被引：71

作者：

Al-Anzi, Bader ^{[1
]}

Sapin, Viveca ^{[1
]}

Waters, Christopher ^{[1
]}

Zinn, Kai ^{[1
]}

Wyman, Robert J. ^{[2
]}

Benzer, Seymour ^{[1
]}

机构：

[1] CALTECH, Div Biol, Pasadena, CA 91125 USA

[2] Yale Univ, MCDB, New Haven, CT 06511 USA

来源：

NEURON | 2009年 / 63卷 / 03期

关键词：

TARGETED GENE-EXPRESSION; MALE COURTSHIP BEHAVIOR; NEUROPEPTIDE-Y; GRYLLUS-BIMACULATUS; SEROTONIN NEURONS; INSULIN-RECEPTOR; NERVOUS-SYSTEM; FRUITLESS GENE; CELL-GROWTH; BODY-WEIGHT;

D O I：

10.1016/j.neuron.2009.07.021

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：329 / 341

页数：13

共 46 条

[11] Attenuation of the obesity syndrome of ob/ob mice by the loss of neuropeptide Y [J].