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Hepatic GCGR activation stimulates gluconeogenesis while simultaneously reducing hepatic fat content through inhibition of de novo lipogenesis and promotion of mitochondrial fatty acid oxidation

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In both in vivo patient-derived xenograft models and in vitro patient-derived organoid models, high-MCU PDAC show increased sensitivity to SLC7A11 inhibition compared to low-MCU tumors, 163 suggesting that MCU-mediated ferroptosis could serve as a therapeutic strategy to prevent PDAC tumor metastasis

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Individual response varies, and not all patients are candidates.