ArticlePloS one2026
Metformin modulates survival, oxidative stress, and gene expression in a high-sucrose Drosophila diabetes model.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundExcess dietary sugar is a major contributor to metabolic disorders, including type 2 diabetes mellitus (T2DM). This study investigates the physiological, biochemical, behavioral, and molecular effects of high-sucrose diets in Drosophila melanogaster and evaluates the modulatory effects of metformin under these conditions.
methodsFlies were reared on normal and high-sucrose diets (5% and 15%), with or without metformin treatment (5 mM and 15 mM). Pupation, survival, locomotor activity (negative geotaxis), trehalose levels, antioxidant enzyme activities (SOD, GST), and expression of stress-related genes (Mn-SOD, Cu/Zn-SOD, MTH, CAT, Hsp40, Hsp70) were assessed after 10 days of treatment. Gene expression levels were quantified relative to the normal control group using RpS20 as the housekeeping reference.
resultsHigh-sucrose diets significantly reduced pupation and survival rates, impaired locomotor performance, increased trehalose levels, and decreased antioxidant enzyme activities. These diets were also associated with downregulation of stress- and antioxidant-related genes. Metformin treatment partially attenuated several of these alterations relative to the corresponding sucrose-treated groups, including improvements in pupation, survival, locomotor performance, metabolic parameters, antioxidant enzyme activity, and gene expression.
conclusionHigh-sucrose diets induced metabolic disturbances in Drosophila melanogaster, including impaired developmental progression and survival, functional locomotor impairment, carbohydrate imbalance, oxidative stress, and suppression of stress-related gene expression. Metformin partially attenuated several of these changes within the corresponding sucrose-treatment groups. These findings support the utility of Drosophila melanogaster as a tractable model for studying diet-induced metabolic dysfunction and evaluating pharmacological interventions.
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