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Dietary Bioactive Components (Poster Session)

(P04-032-24) Effect of High-Fat Diet-Induced Obesity on the Metabolism of (-)-Epigallocatechin-3-Gallate at Non-Toxic and Toxic Doses in Mice

Sunday, June 30, 2024
11:45 AM – 12:45 PM CT
Location: Poster Board 108

    Presenting Author(s)

  • SH

    Soomee Hwang, MS

    Graduate Student
    The Pennsylvania State University
    State College, Pennsylvania, United States

    • Co-Author(s)

  • IK

    Imhoi Koo

    The Pennsylvania State University, United States

  • AP

    Andrew D. Patterson

    The Pennsylvania State University

  • JL

    Joshua D. Lambert, PhD

    Professor
    The Pennsylvania State University
    University Park, Pennsylvania, United States

Disclosure(s):
Soomee Hwang: No relevant financial relationship(s) with ineligible companies to disclose.


Objectives: With the rising prevalence of obesity, green tea-based dietary supplements have gained popularity due to their potential to mitigate obesity. However, studies have reported that oral bolus doses of (-)-epigallocatechin-3-gallate (EGCG), the most abundant catechin in green tea, have the potential to induce hepatotoxicity. The underlying mechanism of the toxicity is unclear, but it has been reported that changes in EGCG metabolite profile may contribute to the toxicity. Given that obesity can affect the activity of phase Ⅱ enzymes, obesity may alter EGCG metabolism and toxicity. This study aimed to investigate how high-fat diet (HFD)-induced obesity affect the EGCG metabolism at non-toxic and toxic doses using a mouse model.

Methods: Male 4-week-old C57BL6/J mice fed a HFD (60% kcal fat) for 10 weeks to induce obesity or a low-fat diet (10% kcal fat). Mice were then given a single intragastric dose of EGCG (non-toxic dose, 100 mg/kg; toxic dose, 750 mg/kg) or vehicle. The urine samples were collected overnight after treatment. We used liquid chromatography-mass spectrometry-based metabolomics to compare the urinary EGCG metabolite profile.

Results: EGCG metabolites were tentatively identified based on their mass to charge (m/z) ratio and fragmentation patterns. Partial least squares discriminant analysis showed that diet was the main driver of the separation of urinary metabolite profiles, and that HFD group with toxic dose was separated from other groups. The glucuronidation and sulfation pathways increased the most with dose in the low-fat and high-fat diet groups, respectively. The HFD group with toxic dose showed higher concentrations of EGCG oxidation products.

Conclusions: The observed differences in metabolite formation between treatment groups indicate that the major biotransformation pathway of EGCG may change with HFD-induced obesity in mice. The presence of high concentrations of EGCG oxidation products in the HFD group given a toxic dose of EGCG suggests that excessive oxidative stress may be induced under a pre-existing obesity condition. To better understand the mechanism under the observed differences in EGCG metabolism, further studies on analyzing the expression and/or activity of metabolizing enzymes are needed.

Funding Sources: USDA Hatch Grant