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The decreased levels of portal insulin, provided there is still portal flow at all in end-stage cirrhosis, make the remaining hepatocytes even more GH-resistant [8]

Its key feature lies in the competitive utilization of the same substrate by iNOS (also known as Nos2) and Arg1: the former generates NO and is closely associated with pro-inflammatory effects, whereas the latter produces ornithine and polyamines and participates in tissue repair and immune regulation ( Under classical pro-inflammatory stimulation (such as LPS/IFN-), iNOS expression is upregulated and catalyzes the conversion of Arg into NO and citrulline

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[DOI] [PMC free article] [PubMed] [Google Scholar] 85.Wu M Yang Z Zhang C Shi Y Han W Song S, et al