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Further, targeted metabolomics and isotope tracing experiments uncovered GGCT as a metabolic orchestrator to prioritize Gln to GSH flux for antioxidant defense, while activating glucose (Glc)-fueled anaplerosis to replenish TCA intermediates to fuel proliferation

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This absence of DEG in cagrilintide and sCT-treated WT mice prevented us to perform a complete analysis of the datasets and compare differences in DEGs between treatment and genotype in the DVC and LPBN