内分泌学
内科学
餐后
肠内分泌细胞
胰高血糖素样肽-1
交感神经系统
肾上腺素能的
内生
葡萄糖稳态
受体
生物
医学
糖尿病
2型糖尿病
内分泌系统
激素
胰岛素抵抗
血压
作者
Wenran Ren,Jianhui Chen,Wenjing Wang,Qingqing Li,Xia Yin,Guanglei Zhuang,Hong Zhou,Wenwen Zeng
出处
期刊:Neuron
[Elsevier]
日期:2024-01-21
卷期号:112 (6): 972-990.e8
被引量:3
标识
DOI:10.1016/j.neuron.2023.12.012
摘要
Summary
Glucose homeostasis is controlled by brain-gut communications. Yet our understanding of the neuron-gut interface in the glucoregulatory system remains incomplete. Here, we find that sympathetic nerves elevate postprandial blood glucose but restrict brain glucose utilization by repressing the release of glucagon-like peptide-1 (GLP-1) from enteroendocrine L cells. Sympathetic nerves are in close apposition with the L cells. Importantly, sympathetic denervation or intestinal deletion of the adrenergic receptor α2 (Adra2a) augments postprandial GLP-1 secretion, leading to reduced blood glucose levels and increased brain glucose uptake. Conversely, sympathetic activation shows the opposite effects. At the cellular level, adrenergic signaling suppresses calcium flux to limit GLP-1 secretion upon sugar ingestion. Consequently, abrogation of adrenergic signal results in a significant improvement in learning and memory ability. Together, our results reveal a sympathetic nerve-enteroendocrine unit in constraining GLP-1 secretion, thus providing a therapeutic nexus of mobilizing endogenous GLP-1 for glucose management and cognitive improvement.
科研通智能强力驱动
Strongly Powered by AbleSci AI