Nutrients · 2025
The Incretin Effect of Yerba Maté (Ilex paraguariensis) Is Partially Dependent on Gut-Mediated Metabolism of Ferulic Acid.
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Cooper-Leavitt Elijah T, Shin Marley J, Beus Colson G, Chiu Alden T, Parker Genevieve, Radford Jack H, Evans Ethan P, Edwards Isaac T, Arroyo Juan A, Reynolds Paul R, Bikman Benjamin T
Аннотация
BACKGROUND/OBJECTIVES: Yerba maté (YM), a traditional herbal beverage made from Ilex paraguariensis, contains bioactive compounds like polyphenols and alkaloids known for their metabolic benefits. This study investigates YM's incretin effects, focusing on glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP). Methods: Male and female C57BL/6 mice were supplemented with YM for four weeks. Post-supplementation, GLP-1 and GIP gene expression levels were analyzed in jejunal mucosa, and plasma hormone concentrations were measured. Additionally, in vitro experiments were conducted using GLUTag L-cells to evaluate the direct effects of YM and its metabolites, including ferulic acid and dihydroferulic acid, on GLP-1 secretion. Gene expression analysis involved quantitative real-time PCR, while hormone levels were assessed via ELISA.
RESULTS: YM supplementation significantly increased GLP-1 gene expression and plasma GLP-1 levels compared to controls, with no changes observed in GIP expression or plasma levels. Direct treatment of GLUTag L-cells with YM did not enhance GLP-1 secretion. However, dihydroferulic acid, a microbial metabolite of ferulic acid, markedly stimulated GLP-1 production in L-cells, highlighting a role of gut-mediated metabolism in YM's incretin effects.
CONCLUSIONS: YM selectively upregulates GLP-1 pathways without affecting GIP, likely through gut-mediated mechanisms. These findings suggest YM as a promising nutraceutical for incretin modulation and metabolic disorder management. Further studies should explore the interplay between YM, the gut microbiota, and incretin pathways to fully realize its therapeutic potential.
RESULTS: YM supplementation significantly increased GLP-1 gene expression and plasma GLP-1 levels compared to controls, with no changes observed in GIP expression or plasma levels. Direct treatment of GLUTag L-cells with YM did not enhance GLP-1 secretion. However, dihydroferulic acid, a microbial metabolite of ferulic acid, markedly stimulated GLP-1 production in L-cells, highlighting a role of gut-mediated metabolism in YM's incretin effects.
CONCLUSIONS: YM selectively upregulates GLP-1 pathways without affecting GIP, likely through gut-mediated mechanisms. These findings suggest YM as a promising nutraceutical for incretin modulation and metabolic disorder management. Further studies should explore the interplay between YM, the gut microbiota, and incretin pathways to fully realize its therapeutic potential.