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Combined intestinal loss of PPAR// attenuates KD-driven intestinal stem cell expansion, proliferation and clonogenicity, whereas inhibition of downstream fatty acid oxidation through CPT1A loss limits adenoma formation specifically under KD, linking tumour initiation to fatty acid oxidation of dietary lipids rather than lipid accumulation

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The primary risk with GHK-Cu is sourcing quality, as unregulated peptide products may contain impurities that cause reactions attributable to contamination rather than the peptide itself

Non-significant paths and non-significant indicators are deleted from the model