Results from five meta-analyses of RCTs evaluating the efficacy of green tea products on glycemic outcomes, oxidative and inflammatory markers in T2DM patients.
| Reference | Number of studies/patients included | Intervention/dosage form/doses | T2DM outcomes | Conclusions | Study limitations |
|---|---|---|---|---|---|
| Dehzad et al. [67] (2025) | 38 RCTs/n = 1,985 | Green tea extracts/infusions/200 mg/day (green tea extract) or 9 g/day (green tea leaves) | Supplementation significantly improved oxidative stress markers, including MDA, TAC, sulfoxide dismutase, and GPX levels in T2DM patients. No significant effects were observed on CRP, IL-6, or TNF-α. | Green tea reduced markers of oxidative stress. Green tea had no effect on inflammatory markers. | Significant heterogeneities in the RCTs, products used and patient characteristics. Included healthy patients, patients with prediabetes, T2DM and other disease states.Low to very low-quality studies included. RCTs on multiple disease states including T2DM. |
| Jia et al. [69] (2024) | 15 RCTs/n = 722 subjects | Green tea, caffeinated and decaffeinated tea/infusions and extracts | Supplementation significantly improved FBG and HbA1c. In T2DM patients, green tea supplements reduced the body mass index and IR. | Consumption of green tea improved FBG levels, HbA1c, and IR in T2DM patients. | Only analyzed the effect of green tea on the glycemic control indexes of T2DM patients, but no other parameters.Some of the extracted data was converted by software, which may have resulted in deviations from the original data.Significant heterogeneity as different green tea preparations were used, different intervention times, and doses were used. |
| Asbaghi et al. [68] (2021) | 14 RCTs/Not stated | Green tea/extracts and infusions/Not stated | Analysis found that green tea did not have a significant impact on FBG, fasting insulin levels, HbA1c, or HOMA-IR. | Green tea had no significant effects on parameters of glycemic control in patients with T2DM. | Significant heterogeneity in the patient populations, intervention duration, intervention times, and dosage. |
| Asbaghi et al. [70] (2019) | 8 RCTs/614 subjects | Green tea/extracts and infusions | Significantly reduced CRP but no significant effect on TAC and MDA. | Green tea consumption reduced CRP but did not reduce oxidative stress in T2DM patients. | A small number of clinical trials and subject included.Significant heterogeneity in intervention duration, intervention times, and dosage. |
| Wang et al. [71] (2014) | 7 RCTs/510 subjects | Green tea/ extracts and infusions | Results showed no statistical difference in FBG, serum insulin, 2-h plasma glucose tolerance test, HbA1c, or IR. | Supplementation with green tea did not decrease the levels of FBG, insulin, HbA1c, or other parameters in subjects at risk for T2DM. | A small number of clinical trials and patients were included in the analysis. Poor methodologies in some of the included RCTs. Significant heterogeneity in the intervention, dose, and study design. Data quality was graded as “very low to low” due to small sample sizes, short duration of treatment (4 weeks–6 months), and methodological deficiencies. Studies included in English and Chinese only. |
CRP: C-reactive protein; FBG: fasting blood glucose; GPX: glutathione peroxidase; HbA1c: glycated hemoglobin; HOMA-IR: homeostasis model assessment of insulin resistance; MDA: malondialdehyde; RCTs: randomized controlled trials; ROS: reactive oxygen species; SOD: superoxide dismutase; T2DM: type 2 diabetes mellitus; TAC: total antioxidant capacity.
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SMW: Investigation, Writing—original draft, Writing—review & editing. TOL: Validation, Writing—review & editing. BAA: Investigation, Validation, Writing—original draft, Writing—review & editing. GPA: Investigation, Writing—review & editing. GBM: Conceptualization, Investigation, Writing—original draft, Writing—review & editing. All authors read and approved the submitted version.
The authors declare that they have no conflicts of interest.
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All information and data in this review are in the public domain. The primary data for this systematic review were sourced online from databases listed in the methods. Referenced articles are accessible on Cochrane Library, PubMed Central/Medline, Embase, Google Scholar, and the Scopus electronic databases. Additional supporting data are available from the corresponding author upon request.
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