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Mechanistically, A42 disrupts LONP1 function through dual pathways: (1) by inhibiting METTL3-mediated LONP1 mRNA m 6 A to negatively regulate LONP1 expression, and (2) by directly binding to LONP1, inducing conformational changes in the protease complex, thereby markedly inhibiting its oligomerization process and substrate hydrolytic activity

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Forman et al., 2009: Glutathione: overview of its protective roles, measurement, and biosynthesis)

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In contrast, another study demonstrated that transgenic mice with a beta-cell specific deletion of the GLP-1R have impaired intraperitoneal (ip) glucose tolerance but maintain normal oral glucose tolerance (Smith et al., 2014)