Min Soohong, Chung Jongkyeong
National Creative Research Initiatives Center for Energy Homeostasis Regulation, Institute of Molecular Biology and Genetics and School of Biological Sciences, Seoul National University, Seoul 08826, Korea.
BMB Rep. 2016 Mar;49(3):137-8. doi: 10.5483/bmbrep.2016.49.3.046.
Satiety cues a feeding animal to cease further ingestion of food, thus protecting it from excessive energy gain. Impaired control of satiety is often associated with feeding-related disorders such as obesity. In our recent study, we reported the identification of a neural pathway that expresses the myoinhibitory peptide (MIP), critical for satiety responses in Drosophila. Targeted silencing of MIP neuron activity strikingly increased the body weight (BW) through elevated food intake. Similarly, genetic disruption of the gene encoding MIP also elevated feeding and BW. Suppressing the MIP pathway behaviorally transformed the satiated flies to feed similar to the starved ones, with augmented sensitivity to food. Conversely, temporal activation of MIP neuron markedly reduced the food intake and BW, and blunted the sensitivity of the starved flies to food as if they have been satiated. Shortly after termination of MIP neuron activation, the reduced BW reverted to the normal level along with a strong feeding rebound. Together our results reveal the switch-like role of the MIP pathway in feeding regulation by controlling satiety. [BMB Reports 2016; 49(3): 137-138].
饱腹感提示进食动物停止进一步摄取食物，从而保护其避免能量过度增加。饱腹感控制受损通常与肥胖等进食相关疾病有关。在我们最近的研究中，我们报告了一条表达肌抑制肽（MIP）的神经通路的鉴定，该通路对果蝇的饱腹感反应至关重要。靶向沉默MIP神经元活性通过增加食物摄入量显著增加体重（BW）。同样，编码MIP的基因的遗传破坏也增加了进食量和体重。抑制MIP通路会使饱腹的果蝇在行为上转变为像饥饿果蝇一样进食，对食物的敏感性增强。相反，MIP神经元的短暂激活显著减少了食物摄入量和体重，并减弱了饥饿果蝇对食物的敏感性，就好像它们已经饱腹一样。MIP神经元激活终止后不久，体重下降恢复到正常水平，同时出现强烈的进食反弹。我们的研究结果共同揭示了MIP通路在通过控制饱腹感调节进食中的开关样作用。[《BMB报告》2016年；49(3):137 - 138]
