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Epigallocatechin gallate increases fatty acid oxidation but not 24-hour survival in lipopolysaccharide-induced endotoxic shock in mice
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Takayuki Irahara, Ryusuke Katsuki, Dai Oishi, Tsuguaki Terashima, Monirul Islam, Umme Salma, Shohag Majumder, Ridwan Ahmed, Eizo Watanabe
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Received October 17, 2025 Accepted February 20, 2026 Published online March 17, 2026
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DOI: https://doi.org/10.15747/ACNM.25.0036
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 Abstract
- Purpose
This study aimed to explore the effects of epigallocatechin gallate (EGCG) in critically ill patients using a mouse model.
Methods
C57BL/6 mice were divided into control and EGCG groups (n=8 per group). The EGCG group received a 0.1% EGCG solution for 2 weeks, after which the mice were intraperitoneally injected with a lethal dose of lipopolysaccharide to induce acute endotoxic shock. Indirect calorimetry was performed for 24 hours. Changes in body weight, epididymal fat weight, and survival were measured, together with serum lipid levels, interleukin-6 (IL-6), and superoxide dismutase (SOD) concentrations. The expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) was determined using quantitative real-time polymerase chain reaction, and its serum concentration was subsequently measured.
Results
Indirect calorimetry showed a significant increase in fatty acid oxidation (P<0.0001) in the EGCG group, along with significant decreases in body weight and epididymal fat weight (P<0.01 and P<0.05, respectively). Survival did not differ significantly between groups (P=0.197). Serum lipid levels, IL-6, and SOD showed numerical differences, although these differences were not statistically significant. Furthermore, hepatic PGC-1α expression showed a tendency toward upregulation, and serum PGC-1α levels were significantly higher (P<0.05).
Conclusion
EGCG stimulates endogenous lipid metabolism through PGC-1α activation and may suppress inflammatory responses; therefore, it may represent a potentially useful nutrient for acute nutritional therapy.
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