Estrogen receptor-α expressing neurons in the ventrolateral VMH regulate glucose balance

Yanlin He, Pingwen Xu, Chunmei Wang, Yan Xia, Meng Yu, Yongjie Yang, Kaifan Yu, Xing Cai, Na Qu, Kenji Saito, Julia Wang, Ilirjana Hyseni, Matthew Robertson, Badrajee Piyarathna, Min Gao, Sohaib A. Khan, Feng Liu, Rui Chen, Cristian Coarfa, Zhongming Zhao, Qingchun Tong, Zheng Sun and Yong Xu ()
Additional contact information
Yanlin He: Baylor College of Medicine
Pingwen Xu: Baylor College of Medicine
Chunmei Wang: Baylor College of Medicine
Yan Xia: Baylor College of Medicine
Meng Yu: Baylor College of Medicine
Yongjie Yang: Baylor College of Medicine
Kaifan Yu: Baylor College of Medicine
Xing Cai: Baylor College of Medicine
Na Qu: Baylor College of Medicine
Kenji Saito: Baylor College of Medicine
Julia Wang: Baylor College of Medicine
Ilirjana Hyseni: Baylor College of Medicine
Matthew Robertson: Baylor College of Medicine
Badrajee Piyarathna: Baylor College of Medicine
Min Gao: Baylor College of Medicine
Sohaib A. Khan: University of Cincinnati, College of Medicine
Feng Liu: University of Texas Health at San Antonio
Rui Chen: Baylor College of Medicine
Cristian Coarfa: Baylor College of Medicine
Zhongming Zhao: The University of Texas Health Science Center at Houston
Qingchun Tong: University of Texas Health Science Center at Houston
Zheng Sun: Baylor College of Medicine
Yong Xu: Baylor College of Medicine

Nature Communications, 2020, vol. 11, issue 1, 1-13

Abstract: 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 report that estrogen receptor-α (ERα)-expressing neurons in the ventrolateral subdivision of the ventromedial hypothalamic nucleus (vlVMH) can sense glucose fluctuations, being glucose-inhibited neurons (GI-ERαvlVMH) or glucose-excited neurons (GE-ERαvlVMH). Hypoglycemia activates GI-ERαvlVMH neurons via the anoctamin 4 channel, and inhibits GE-ERαvlVMH neurons through opening the ATP-sensitive potassium channel. Further, we show that GI-ERαvlVMH neurons preferentially project to the medioposterior arcuate nucleus of the hypothalamus (mpARH) and GE-ERαvlVMH neurons preferentially project to the dorsal Raphe nuclei (DRN). Activation of ERαvlVMH to mpARH circuit and inhibition of ERαvlVMH to DRN circuit both increase blood glucose. Thus, our results indicate that ERαvlVMH neurons detect glucose fluctuations and prevent severe hypoglycemia in mice.

Date: 2020
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DOI: 10.1038/s41467-020-15982-7

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