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Blocking the catalytic breakdown of GLP-1 and GIP, allows for postprandial insulin release [44]
This selective action means it primarily targets growth hormone release, leaving other hormones like cortisol, prolactin, and aldosterone largely unaffected
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demonstrated that GLP-1 activates the cAMP/PKA signaling pathway by binding to its receptor GLP-1R and by then phosphorylating the PKA consensus site of NHE3 (101)
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