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This demonstrates that GLP-1R agonism also regulates (mostly reducing) ethanol-metabolizing genes, which are independent of ethanol intake

Mechanistically, macrophage-specific inhibition of GLUL leads to accumulation of succinate and HIF-1 via glutamine-dependent -aminobutyric acid (GABA) shunting (thereby inhibiting vessel sprouting and metastasis) and via stimulation of T effector cells