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Treating the molecule as a single story misses what the trials actually say

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[3] Some of these effects have been demonstrated with systemic administration in animals, which is the strongest mechanistic basis for the idea that injected GHK-Cu could do something systemically

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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