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Glucagon-like peptide-1 mobilizes intracellular Ca2+ and stimulates mitochondrial ATP synthesis in pancreatic MIN6 -cells

the shared incretin endpoint shows why that too is false

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Among the numerous major discoveries made in this regard was the finding that the hyperglycemic effect of glucagon resides in its ability to act in the liver to stimulate glycogenolysis and gluconeogenesis [[6], [7], [8], [9], [10], [11], [12]] despite its seemingly paradoxical ability to stimulate insulin secretion in humans reported by Ellis Samols in 1965 [13]

Gut microbiota-derived metabolites, such as short-chain fatty acids (SCFAs), tryptophan metabolites, and immune stimulants, are likely mediators in this process [85]

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