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In particular, dysregulation of the gut-liver-muscle-brain axis, driven by hyperammonemia, systemic inflammation, sarcopenia, altered bile acid signaling, and gut dysbiosis, plays an important role in the pathogenesis and progression of CHE [9, 10]

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GLP-1R Trp 78 , Pro 90 , Trp 91 , and His 212 could form a hydrophobic region with GLP-1 Phe 28 , Ile 29 , Trp 31 , Leu 32 , and Val 33 , and GIPR Leu 35 , Trp 39 , Tyr 36 , Met 67 , Tyr 87 , Trp 90 , and His 115 could form a hydrophobic region with GIP Phe 22 , Val 23 , Trp 25 , Leu 26 , and Leu 27

There are also studies investigating an effect of metal chelators and dietary approaches aimed at reducing intake of iron and copper [6]