5月28日【FIBS】清华大学生物论坛“云上学术”系列讲座之第3期预告

时间：2020-05-28 10:00-11:00

主讲人：Prof.Yong Xu（Baylor college of medicine）

主题：Central control of metabolism: Does sex truly matter?

会议方式:腾讯会议(ID:894741872,https://meeting.tencent.com/l/57T4g6Pd44d4)

Biography

Dr. Xu obtained his medical degree in Tongji Medical University (China) and then Ph.D. degree in University of Alberta (Canada). After a postdoctoral training at the University of Texas Southwestern Medical Center (Dallas), he established his own research program at Baylor College of Medicine in 2010. The major goals of Dr. Xu's lab are to identify the novel neural circuits, neurotransmitters and intracellular molecules in the brain that are critical for control of energy and glucose homeostasis. Dr. Xu’s group uses Cre-loxP/Flp-frt mouse models, in combination of chemogenetics/optogenetics, neuroanatomy, neurotracing and electrophysiology, to establish the physiological relevance of specific neural networks in the regulation of feeding behavior, energy metabolism and glucose balance. Dr. Xu’s research has been continuously funded by various sources, including USDA, NIH, AHA, and ADA, etc. Dr. Xu is a recipient of Michael E. DeBakey, M.D. Excellence in Research Award, Molecular and Cellular Biology Excellence in Research Award, and Pediatrics Research Mentor Award.

Abstract

Brain glucose-sensing neurons detect glucose fluctuations and prevent severe hypoglycemia, but mechanisms mediating functions of these glucose-sensing neurons are unclear. Here we show that estrogen receptor-α (ERα)-expressing neurons in the ventrolateral subdivision of the ventromedial hypothalamic nucleus (vlVMH) are glucose-sensing neurons, being glucose-inhibited neurons (GI-ERα^vlVMH) or glucose-excited neurons (GE-ERα^vlVMH). Hypoglycemia activates GI-ERα^vlVMH neurons via the anoctamin 4 channel, and inhibits GE-ERα^vlVMH neurons through opening the ATP-sensitive potassium channel. GI-ERα^vlVMH neurons preferentially project to the medioposterior arcuate nucleus of the hypothalamus (mpARH) and GE-ERα^vlVMH neurons preferentially project to the dorsal Raphe nuclei (DRN). Activation of ERα^vlVMHàmpARH circuit and inhibition of ERα^vlVMHàDRN circuit both increase blood glucose. Depletion of endogenous estrogens in female mice impairs glucose-sensing functions of ERα^vlVMH neurons and deletion of ERα in the vlVMH blunts the counterregulatory responses during hypoglycemia. Thus, our results indicate that ERα^vlVMH neurons detect glucose fluctuations and prevent severe hypoglycemia in female mice.

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