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HGF/c-Met signaling is a well-established oncogenic pathway: c-Met is amplified or overexpressed in multiple cancers (gastric, lung, renal, hepatocellular) HGF/c-Met activation promotes tumor cell proliferation, survival, invasion, and metastasis c-Met inhibitors are FDA-approved cancer drugs (cabozantinib, crizotinib, capmatinib) A compound that potentiates HGF/c-Met signaling raises theoretical concerns about promoting tumor growth or transformation with chronic use

Creatine increases creatinine levelsa waste product that kidneys filterwhile semaglutide can cause dehydration and osmotic shifts that temporarily stress renal function

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Effects of glycogen on ceramide production in cultured human keratinocytes via acid sphingomyelinase activation

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