Regulation of glucose homeostasis is a central feature of antidiabetic drugs such as metformin. However, a subset of individuals exhibited limited therapeutic response, highlighting the need for complementary treatment strategies. Taurine, a semi-essential amino acid, has been reported to improve glycemic control in mammalian models, supporting its potential as an adjuvant therapy for metabolic disorders. In this study, we established a fructose-induced metabolic dysfunction model in Caenorhabditis elegans (C. elegans), characterized by increased intracellular glucose accumulation, and evaluated the effects of taurine. A metabolic dysfunction state was induced in L1-stage N2 Bristol worms by exposing them to 500 mM fructose for 48 h. Metformin (25, 50, and 100 µM) was initially used to establish an effective pharmacological control, and the optimal dose (50 µM) was subsequently employed as a positive control to assess the effects of taurine (10, 50, and 100 µM) under fructose-induced conditions. Fructose exposure significantly increased intracellular glucose levels. Metformin reduced intracellular glucose at all concentrations tested and improved survival at the lowest dose, without affecting morphological parameters. Taurine reduced intracellular glucose accumulation only at the highest concentration tested (100 µM), whereas lower concentrations selectively increased survival, indicating dose-dependent and functionally distinct effects on glucose regulation and organismal viability. These findings show that taurine modulates intracellular glucose accumulation and survival in fructose-treated C. elegans. Given the evolutionary conservation of key pathways involved in glucose metabolism, this model provides a simple and reproducible platform to investigate mechanisms of glucose dysregulation and to screen compounds with potential metabolic or antidiabetic activity.
Machado et al. (Mon,) studied this question.