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within retatrutide's triple-agonist design, this effect is thought to be counterbalanced by concurrent GLP-1 and GIP activity, though this remains under investigation in ongoing trials

Traditionally, microglial activation has been described using the M1/M2 framework, in which M1 corresponds to a proinflammatory profile and M2 to an anti-inflammatory, tissue-repairing state [31]

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