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identified the aryl hydrocarbon receptor (AHR) as the apical mediator of Acteoside s effects in both adenine-induced nephropathy and cellular models of fibrosis ( Acteoside administration not only modulated the Nrf2 and NF-B pathways but also concurrently suppressed AHR nuclear translocation and the expression of its canonical targets (CYP1A1, CYP1A2)

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GLP-1s could mark a positive shift that we are approaching peak consumption

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