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The Y138 1.36b A mutation in GCGR greatly decreased the potency of retatrutide-induced cAMP signaling by 26.9-fold, while Y138 1.36b L moderately increased it, suggesting the hydrophobic interactions at 1.36b play a crucial role (Fig

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In parallel, citrate synthase supports fatty acid biosynthesis, whereas acyl-CoA synthetase family member 2 (ACSF2) contributes to fatty acid activation, providing lipid substrates that can fuel peroxidation reactions [41]

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