Dihydromyricetin preserves β-cell function in type 1 diabetes via PI3K/AKT-mediated metabolic reprogramming.

ABSTRACT:

Background

Food-derived flavonoids are emerging as nutraceutical agents for glycemic control. Dihydromyricetin (DMY), the signature flavanonol of vine tea (Ampelopsis grossedentata), has long been consumed in South China, yet its antidiabetic potential remains underexplored.

Methods

We administered DMY (50 and 100 mg/kg/day, 12 days) to streptozotocin-induced type 1 diabetic mice. Fasting glycemia, lipid panels, and HOMA-β were evaluated 4 weeks after DMY administration. Untargeted UPLC-QTOF metabolomics combined with network pharmacology pinpointed pathway hubs, while experiments in INS-1 β-cells using the PI3K inhibitor LY294002 verified the pathway's involvement.

Results

DMY reduced hyperglycemia, corrected dyslipidemia, and preserved islet architecture. Met

SUBMITTER: Li J 

PROVIDER: S-EPMC12527859 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature