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As the arsenal of incretin therapies targeting glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptors continues to expand, clinicians need to balance the myriad clinical benefits with potentially severe adverse effects (AEs) to put this principle into practice

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GPR43 (FFAR2) shows higher sensitivity to acetate and propionate than to butyrate, whereas GPR41 is primarily activated by propionate and butyrate (65, 66)

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