期刊
SCIENCE ADVANCES
卷 8, 期 23, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abn5345
关键词
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资金
- National Natural Science Foundation of China [31822026, 32100821, 91957112, 31970950]
- Robert Wood Johnson Foundation [74260]
- National Institutes of Health [R01MH116694]
- National Key R&D Program of China [2021ZD0203900]
- Institute of Advanced Technology-Huami Joint Laboratory for Brain-Machine Intelligence at the University of Science and Technology of China
This study identified a population of glucose-sensing GLP-1 receptor neurons in the dorsomedial hypothalamic nucleus, which can decrease blood glucose levels through communication with the pancreas. The mechanism by which this central GLP-1 signal controls glucose levels was also elucidated.
Glucagon-like peptide-1 (GLP-1) regulates energy homeostasis via activation of the GLP-1 receptors (GLP-1Rs) in the central nervous system. However, the mechanism by which the central GLP-1 signal controls blood glucose levels, especially in different nutrient states, remains unclear. Here, we defined a population of glucose-sensing GLP-1R neurons in the dorsomedial hypothalamic nucleus (DMH), by which endogenous GLP-1 decreases glucose levels via the cross-talk between the hypothalamus and pancreas. Specifically, we illustrated the sufficiency and necessity of DMHGLP-1R in glucose regulation. The activation of the DMHGLP-1R neurons is mediated by a cAMP-PKA-dependent inhibition of a delayed rectifier potassium current. We also dissected a descending control of DMHGLP-1R-dorsal motor nucleus of the vagus nerve (DMV)-pancreas activity that can regulate glucose levels by increasing insulin release. Thus, our results illustrate how central GLP-1 action in the DMH can induce a nutrient state-dependent reduction in blood glucose level.
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