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The increased glutathione redox status could be a compensatory mechanism in response to the increased oxidative burden due to anemia and obesity
Another future direction of utilising GLP-1/GIP/glucagon receptor triagonists is for MASH therapy with the rationale that as GLP-1 receptor agonists halt fibrosis progression, the new therapies might be able to enable fibrosis regression [11]
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Endocrinology 140 , 11321140 (1999)
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