Journal of Agriculture and Food Research · Jul 30, 2026

Ameliorative effects and mechanisms of Crataegus pinnatifida leaf extract on high-sugar diet-induced metabolic dysregulation in Drosophila melanogaster

By Fan X, Li J, Abubakar M et al.

: Chronic consumption of sugar-rich diets is a major contributor to metabolic disorders, particularly type 2 diabetes mellitus (T2DM). Crataegus pinnatifida leaf (CPL) have attracted increasing attention as potential functional food ingredients; however, the mechanisms underlying their antidiabetic activity remain insufficiently defined. In this study, the phytochemical profile of CPL was characterized by UHPLC-Q-Orbitrap-MS/MS, and its antidiabetic effects were evaluated using in vitro enzyme inhibition assays combined with a high-sugar diet (HSD)-induced Drosophila melanogaster model. A total of 105 compounds were identified, including 46 flavonoids, with hyperoside, neosmitilbin, scutellarin, glabrone, and rutin as the predominant constituents. CPL exhibited strong inhibitory activities against α-amylase (IC 50 = 0.229 ± 0.011 mg/mL) and α-glucosidase (IC 50 = 0.047 ± 0.001 mg/mL) in vitro . In vivo , CPL supplementation significantly ameliorated the HSD-induced T2DM-like phenotype, as evidenced by reduced whole-body glucose and triglyceride levels, improved growth and developmental parameters, and extended lifespan. Transcriptomic analysis and RT-qPCR validation further indicated that these effects were associated with coordinated changes in the expression of genes involved in conserved nutrient-sensing pathways, particularly insulin/insulin-like growth factor signaling (IIS), forkhead box O (FoxO), and target of rapamycin (TOR) signaling, and these findings were supported by protein-level validation showing that CPL restored Akt phosphorylation. Overall, these findings provide molecular mechanistic insights supporting Crataegus pinnatifida leaf as a promising natural functional food ingredient for mitigating diet-induced metabolic disorders.

doi.org/10.1016/j.jafr.2026.103185Open accessInterventions

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