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These data suggest that GLP-1 receptors contribute to the insulinotropic action of glucagon and that in GLP-1R knockout mice there is some extrapancreatic mechanism that compensates for the loss of glucagon-induced insulin secretion via GLP-1R
This represents a precautionary approach rather than a requirement based on proven deficiency risk
Patent filings mirror this escalation, with claims covering dosing regimens and compositions for tri-agonists and next-wave combinations [5, 6]
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