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The oral form uses a SNAC (sodium N-[8-(2-hydroxybenzoyl)amino]caprylate) absorption enhancer to allow GLP-1 passage through the gastric mucosa, achieving approximately 1% bioavailability compared to subcutaneous injection

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Here, working primarily in mouse hepatocytes, we show that decreasing the availability of substrate for the TCA cycle diminished NADPH production and attenuated ER stress in a manner that depended on glutathione oxidation

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Moreover, emerging research suggests that targeting both the GLP-1 and GIP pathways may lead to synergistic effects on body weight, glucose control, and cardiovascular health