reported that GLP-1-induced suppression of glucagon release is dependent of protein kinase A (PKA) and independent of glucose or paracrine effects mediated by insulin or by somatostatin acting on somatostatin receptor subtype-2 [16],[17]
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Lactate promotes endothelial-to-mesenchymal transition via Snail1 lactylation after myocardial infarction
ACSL4 can catalyze the esterification of PUFAs in phospholipids on cellular membranes and enhance ferroptosis sensitivity to lipid peroxidation (Zhang et al., 2025c)
A key initial concern of using glucagon within a co-agonist was unwanted hyperglycaemia
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