报告人：何彦林 博士，Children’s Nutrition Research Center, Baylor College of Medicine
Yanlin He, Ph.D., received a bachelor's degree from Nanchang University in 2007. He received his Ph.D. degree from Fudan University in 2012 with the main research interest in biophysics. From 2012 to 2014, he worked as a postdoctoral in University of Connecticut Health Center, USA. Now he also works as a postdoctoral in Children’s Nutrition Research Center, Baylor College of Medicine, USA. Representative works were published in Nature Medicine, Nature Neuroscience, Cell Reports, Nature Communications, and so on.
Neurons that co-express agouti-related peptide (AgRP) and neuropeptide Y (NPY) are indispensable for normal feeding behavior. Firing activities of AgRP/NPY neurons are dynamically regulated by energy status and coordinate appropriate feeding behavior to meet nutritional demands. However, intrinsic mechanisms that regulate AgRP/NPY neural activities during the fed-to-fasted transition are not fully understood. We found that AgRP/NPY neurons in satiated mice express high levels of the small-conductance calcium-activated potassium channel 3 (SK3) and are inhibited by SK3-mediated potassium currents; on the other hand, food deprivation suppresses SK3 expression in AgRP/NPY neurons, and the decreased SK3-mediated currents contribute to fasting-induced activation of these neurons. Genetic mutation of SK3 specifically in AgRP/NPY neurons leads to increased sensitivity to diet-induced obesity, associated with chronic hyperphagia and decreased energy expenditure. Our results identify SK3 as a key intrinsic mediator that coordinates nutritional status with AgRP/NPY neural activities and animals' feeding behavior and energy metabolism.
报告联系人: 1808组 许国旺