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GLP-1RAs, such as lixisenatide, not only rely on -cell function and glucagon suppression, but also assist to lower glucose by other (insulin-independent) mechanisms such as delayed gastric emptying, underlying the clinical utility of GLP-1RAs as adjuvant therapy to basal insulin in longstanding T2DM [14]
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Firstly, at the molecular expression level, TMAO can significantly up-regulate the expression of MHC-II molecules and co-stimulatory molecules CD86 on the surface of DCs
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