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The reasonable scientific conclusion is that CagriSema is a promising but unproven candidate for obesity-related liver disease: mechanistically coherent, backed by strong component-level (semaglutide) human data and preclinical amylin signals, yet lacking any direct combination trial in liver disease
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If paracrine/autocrine IGF-I production is lost in addition to liver-derived IGF-I, the metabolic consequences become obvious
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