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While the mechanisms responsible for these potent effects remain incompletely understood, contributors include altered postprandial nutrient delivery to the intestine, increased secretion of glucagon-like peptide 1 (GLP-1) by intestinal L cells, increased insulin secretion, intestinal mucosal adaptations, alterations in the gut-brain axis, and changes in bile acid content and composition (3, 4)
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No code was used or generated in this study
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