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Neurons, astrocytes, oligodendrocytes, microglia, endothelial cells, and pericytes all express GLP-1 receptors, positioning incretin signaling to influence neuronal metabolism, synaptic support, neuroinflammation, myelination, vascular integrity, and bloodbrain barrier function [22]

ABCG2 dysfunction caused by common variants will significantly increase the risk of hyperuricaemia, and the reduction of extra renal urate excretion through dysfunctional ABCG2 is a common mechanism of hyperuricaemia (Ichida et al., 2012)

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However, a single pulse light stimulation of PPG neurons produces only glutamatergic EPSCs, but not IPSCs, in granule cells

By mimicking the bodys endogenous GLP-1, these drugs suppress appetite, slow gastric emptying, and influence reward mechanisms in the brain

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