Taurine alleviates endoplasmic reticulum stress, oxidative stress, apoptosis, and glycogen accumulation induced by high glucose in the muscle cells of golden pompano (Trachinotus ovatus).

High-glucose environments induce cellular stress, particularly endoplasmic reticulum stress (ERS) and oxidative stress, in aquatic animals. Taurine, known for its cell-protective properties, has potential in mitigating such stress. This study investigated taurine's effects on ERS, oxidative stress, apoptosis, and glycogen accumulation in golden pompano (Trachinotus ovatus) muscle cells under high-glucose conditions. Cells were cultured with varying glucose concentrations and taurine supplementation. Techniques including Cell Counting Kit-8 (CCK-8) assay, Nile Red staining, periodic acid-Schiff (PAS) staining, and transmission electron microscopy (TEM) were used to assess cell viability, lipid deposition, glycogen accumulation, and ultrastructural changes, respectively. High glucose increased the ADP/ATP ratio, reactive oxygen species (ROS) levels, and reduced mitochondrial membrane potential (MMP), activating AMP-activated protein kinase (AMPK). This led to glycogen accumulation via increased glycogen synthase (gysm) expression and decreased glycogen phosphorylase (pygm) expression. Taurine supplementation restored glycogen balance, reduced glucose transporter 4 (GLUT4) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) protein levels, and alleviated ERS, as evidenced by reduced PKR-like ER kinase (perk) mRNA and glucose-regulated protein 78 (GRP78) protein expression. Also, taurine improved mitochondrial function, inhibiting apoptosis by reducing cytochrome C (CytC) release. In conclusion, taurine alleviated ERS, glycogen accumulation, apoptosis, and mitochondrial oxidative stress, providing new insights into taurine's mechanisms and supporting its potential use as a feed additive in aquaculture. Supplementary Information: The online version contains supplementary material available at 10.1007/s42995-025-00324-7.