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As we look ahead, its clear that understanding the impact of these therapies will be essential for shaping the future of healthcare, insurance, and public health

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

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)

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]