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In intact murine islets, blockade of N-type Ca 2+ channels with -conotoxin, but not L-type Ca 2+ channels using nifedipine, abolishes low glucose (1 mM) stimulation of glucagon secretion and blunts the GLP-1-mediated inhibitor effects

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Chronic hyperglycemia and hyperinsulinemia drive a metabolic imbalance promoting oxidative stress, inflammation, and endothelial damage, responsible for non-enzymatic biomolecule glycation, accelerating cerebrovascular atherosclerosis and neurodegenerative damage that further promote cognitive dysfunction and dementia (Kopp et al., 2022)

Receptors of these incretins, GLP-1R and GIPR are G protein-coupled receptors (GPCR) that activate the classical signaling cascade through Gs and adenylate cyclase (Adcy), leading to increased cAMP production [6,7]

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It is documented