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In addition to these findings on atherosclerotic plaque formation, GLP-1R agonists prevented the increase in plasminogen activator inhibitor type-1 (PAI-1) and vascular cell adhesion molecule-1 (VCAM-1) gene expression in response to TNF- or hyperglycemia in HUVEC through PKA pathway [24],[70]
A contribution of NTS astrocytes to the appetite suppression caused by acute GLP-1R agonists also seems possible from evidence showing (1) expression of GLP-1Rs in this cell type, (2) functional responses of astrocytes to exendin-4 and liraglutide, and (3) negation of appetite suppression from administration of exendin-4 into the NTS when astrocyte metabolism is selectively inhibited in this region [56]
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This has made KLOW relevant in research focused on inflammation control, tissue stress, and recovery support
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