ArticleNPJ science of food2025
Cyanidin-3-O-glucoside enhances GLP-1 secretion via PPARβ/δ-β-catenin-TCF-4 pathway in type 2 diabetes mellitus.
Article in NPJ science of food, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Mettl14-mediated mJournal of endocrinological investigation · 2026Article
- Liposomal Delivery ofPharmaceutics · 2026Article
- Porous-starch-encapsulated quercetin remodels the gut microbiota and elevates short-chain fatty acids, alleviating hyperglycaemia-associated phenotypes in T2DM mice.Frontiers in nutrition · 2026Article
- Anthocyanins Modulation of Gut Microbiota to Reverse Obesity-Driven Inflammation and Insulin Resistance.Nutrients · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
In late-stage type 2 diabetes mellitus (T2DM), impaired islet β cell function leads to absolute insulin deficiency, thereby disrupting blood glucose homeostasis. GLP-1, an incretin hormone, stimulates insulin secretion from islet β cells post-meals. This study investigated the effects of anthocyanin cyanidin-3-O-glucoside (C3G) on GLP-1 secretion using STC-1 (intestinal endocrine L cells) and NIT-1 (islet β cells). In a co-culture system, C3G treatment increased GLP-1 secretion in STC-1 cells, promoting insulin release in NIT-1 cells under high glucose. Mechanistically, C3G activated the PPARβ/δ-β-catenin-TCF-4 pathway in STC-1 cells, enhancing PG precursor transcription and GLP-1 synthesis.Inhibiting PPARβ/δ with GSK0660 blocked this C3G-induced upregulation. Overall, C3G stimulates GLP-1 secretion from intestinal L cells via this pathway, indirectly boosting insulin release from β cells. These findings enhance T2DM mechanism understanding and suggest the potential of C3G in GLP-1-based T2DM therapy.
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Registered trials
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