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Brain Endothelial Cells Regulate Glucagon-Like Peptide 1 Entry Into the Brain via a Receptor-Mediated Process
被引:38
作者:
Fu, Zhuo
[1
]
Gong, Liying
[1
,2
]
Liu, Jia
[1
]
Wu, Jing
[1
,3
]
Barrett, Eugene J.
[1
]
Aylor, Kevin W.
[1
]
Liu, Zhenqi
[1
]
机构:
[1] Univ Virginia Hlth Syst, Div Endocrinol & Metab, Dept Med, Charlottesville, VA 22903 USA
[2] Cent South Univ, Xiangya Hosp 3, Dept Pharmacol, Changsha, Peoples R China
[3] Cent South Univ, Xiangya Hosp, Dept Endocrinol, Changsha, Peoples R China
基金:
美国国家卫生研究院;
关键词:
Glucagon-like peptide 1;
blood brain barrier;
endothelial cells;
microvasculature;
protein kinase A;
RECRUITS MUSCLE MICROVASCULATURE;
SKELETAL-MUSCLE;
EXPRESSING CELLS;
MESSENGER-RNA;
FOOD-INTAKE;
GLP-1;
PROTEIN;
MODEL;
DELIVERY;
NEURONS;
D O I:
10.3389/fphys.2020.00555
中图分类号:
Q4 [生理学];
学科分类号:
071003 ;
摘要:
Glucagon-like peptide 1 (GLP-1) in addition to regulating glucose-dependent insulin and glucagon secretion exerts anorexic and neuroprotective effects. While brain-derived GLP-1 may participate in these central actions, evidence suggests that peripherally derived GLP-1 plays an important role and GLP-1 analogs are known to cross the blood brain barrier. To define the role of brain microvascular endothelial cells in GLP-1 entry into the brain, we infused labeled GLP-1 or exendin-4 into rats intravenously and examined their appearance and protein kinase A activities in various brain regions. We also studied the role of endothelial cell GLP-1 receptor and its signaling in endothelial cell uptake and transport of GLP-1. Systemically infused labeled GLP-1 or exendin-4 appeared rapidly in various brain regions and this was associated with increased protein kinase A activity in these brain regions. Pretreatment with GLP-1 receptor antagonist reduced labeled GLP-1 or exendin-4 enrichment in the brain. Sub-diaphragmatic vagus nerve resection did not alter GLP-1-mediated increases in protein kinase A activity in the brain. Rat brain microvascular endothelial cells rapidly took up labeled GLP-1 and this was blunted by either GLP-1 receptor antagonism or protein kinase A inhibition but enhanced through adenylyl cyclase activation. Using an artificially assembled blood brain barrier consisting of endothelial and astrocyte layers, we found that labeled GLP-1 time-dependently crossed the barrier and the presence of GLP-1 receptor antagonist blunted this transit. We conclude that GLP-1 crosses the blood brain barrier through active trans-endothelial transport which requires GLP-1 receptor binding and activation.
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页数:12
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