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Animal model studies consistently demonstrated that semaglutide can significantly alter gut microbiota, suggesting that part of semaglutides metabolic benefit may derive from its capacity to modulate inflammation via gut-immune-microbiota interactions and to correct dysbiosis induced by high-fat diets [82, 84]

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No current non-animal system captures this integrated response

In plain terms: the GIP component may let some patients tolerate a more effective dose without as much queasiness, so they actually reach a level that works for them

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