RES supplementation significantly reduced CRP, lipid peroxide levels, and oxidative stress score, and significantly increased GPX levels and catalase levels. No significant effects for IL-6, TNFα, superoxide dismutase levels, total antioxidant capacity, or MDA.
RES supplements had anti-inflammatory effects and reduced oxidative stress. score in T2DM patients.
A limited number of RCTs and a small sample size. Low-quality clinical trials were included in the analyses.Significant heterogeneity exists in the dose and intervention times for RES supplements varied widely.Many studies from Middle Eastern countries, that may reduce generalizability. No subgroup analyses performed.
RES reduced the HOMA-IR, HbA1c, FBG, and fasting insulin levels, which were significantly different. No significant difference in HDL-C, MDA, TC, or TG levels. No significant difference in adverse events between RES and placebo.
RES supplementation may improve insulin resistance, lower fasting blood glucose and insulin levels, and improve oxidative stress in T2DM patients, but has no effect on lipid parameters.
Significant heterogeneity in the data and studies included.Some of the RCTs analyzed were of low methodological quality due to poor randomization methods or blinding. A small number of subjects in some studies. Significant variations in the dose range and duration of RES may have impacted the conclusion and introduced bias.
In T2DM patients, high doses of RES (≥ 1000 mg) reduced FBG, SBP, and DBP. No significant effect was observed for waist circumference, TG, or HDL-C levels.
RES supplementation reduced SBP and DBP in T2DM patients. High dose RES reduced fasting blood glucose but had no significant effect on waist circumference, TGs, or HDL levels.
Significant heterogeneity for the subjects included variation in the dose range and duration of RES treatment. These may have impacted the overall conclusion.
The authors declare that they have no conflicts of interest.
Ethical approval
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Consent to publication
Not applicable.
Availability of data and materials
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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