Endothelial HIF-1α enables hypothalamic glucose uptake to drive POMC neurons.
    
    
        
    
    
        
        Diabetes 66, 1511-1520 (2017)
    
    
    
      
      
	
	    Glucose is the primary driver of hypothalamic POMC neurons. Here, we show that endothelial HIF-1α controls glucose uptake in the hypothalamus, and, that it is up-regulated in conditions of under-nourishment during which POMC neuronal activity is decreased. Endothelium-specific knockdown of HIF-1α impairs the ability of POMC neurons to adapt to the changing metabolic environment in vivo resulting in overeating of mice after food deprivation. The impaired functioning of POMC neurons was reversed ex vivo or by parenchymal glucose administration. These observations indicate an active role for endothelial cells in the central control of metabolism and suggest that central vascular impairments may cause metabolic disorders.
	
	
	    
	
       
      
	
	    
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        Publication type
        Article: Journal article
    
 
    
        Document type
        Scientific Article
    
 
    
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        Keywords
        Agrp Neurons; Leptin Resistance; Brain; Acid; Availability; Transporters; Hif-1-alpha; Homeostasis; Signals; Barrier
    
 
    
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        Language
        english
    
 
    
        Publication Year
        2017
    
 
    
        Prepublished in Year
        
    
 
    
        HGF-reported in Year
        2017
    
 
    
    
        ISSN (print) / ISBN
        0012-1797
    
 
    
        e-ISSN
        1939-327X
    
 
    
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	    Volume: 66,  
	    Issue: 6,  
	    Pages: 1511-1520 
	    Article Number: ,  
	    Supplement: ,  
	
    
 
    
        
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            Publisher
            American Diabetes Association
        
 
        
            Publishing Place
            Alexandria, VA.
        
 
	
        
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        Reviewing status
        Peer reviewed
    
 
     
    
        POF-Topic(s)
        30201 - Metabolic Health
    
 
    
        Research field(s)
        Helmholtz Diabetes Center
    
 
    
        PSP Element(s)
        G-502200-001
    
 
    
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        Erfassungsdatum
        2017-06-13