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Under sustained GLP-1RAinduced hypophagia, oxidative stability may become increasingly dependent on adequate antioxidant and redox-buffering capacity

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In particular, GLP1-RA counteract the action of angiotensin II (ANG II) inhibiting its synthesis, increasing the inactivation of its circulating form and contrasting its action on target tissue like glomerular endothelial cells and cardiomyocytes

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