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However, drugs that provide long-term effects of treatment and/or target later phase after stroke might be more crucial, because a prolonged time-window of treatment applies to most of new victims, as well as dysfunction is persistent in patients with stroke (155)

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A disrupted liveralpha cell axis has been observed in humans with NAFLD, implying that elevated amino acid levels (and potentially fatty acids) as opposed to dysfunctional glucose sensing by the alpha cells are responsible for hyperglucagonaemia [42]