TY - JOUR
T1 - Green tea extract supplementation does not modify plasma concentration of F2-isoprostanes in women who are postmenopause
T2 - Findings from a randomized controlled trial
AU - Bathgate, Jennifer R.
AU - Radler, Diane Rigassio
AU - Kurzer, Mindy
AU - Samavat, Hamed
N1 - Publisher Copyright:
© 2023 Elsevier Inc.
PY - 2023/5
Y1 - 2023/5
N2 - Green tea extract (GTE) is a potential mitigator of oxidative stress, and F2-isoprostanes are a reliable biomarker of oxidative stress. Genetic polymorphisms in the catechol-o-methyltransferase (COMT) gene may modify tea catechin metabolism, prolonging exposure. We hypothesized that GTE supplementation would decrease plasma F2-isoprostanes concentrations compared with placebo and that participants with the COMT genotype polymorphisms would experience a more significant expression of this outcome. This study was a secondary analysis of the Minnesota Green Tea Trial, a randomized placebo-controlled, double-blinded trial investigating the effects of GTE in women who were generally healthy and postmenopausal. The treatment group consumed 843 mg of epigallocatechin gallate daily for 12 months versus placebo. Participants in this study had a mean age of 60 years, were predominantly White, and most had a healthy body mass index. GTE supplementation did not significantly change plasma F2-isoprostanes concentrations compared with placebo after 12 months (P for overall treatment = .07). There were no significant interactions between treatment and age, or body mass index, physical activity, smoking history, and alcohol intake. COMT genotype did not modify the effect of GTE supplementation on F2-isoprostanes concentrations in the treatment group (P = .85). Among participants in the Minnesota Green Tea Trial, consuming GTE supplements daily for 1 year did not result in a significant decrease in plasma F2-isoprostanes concentrations. Likewise, the COMT genotype did not modify the effect of GTE supplementation on F2-isoprostanes concentrations.
AB - Green tea extract (GTE) is a potential mitigator of oxidative stress, and F2-isoprostanes are a reliable biomarker of oxidative stress. Genetic polymorphisms in the catechol-o-methyltransferase (COMT) gene may modify tea catechin metabolism, prolonging exposure. We hypothesized that GTE supplementation would decrease plasma F2-isoprostanes concentrations compared with placebo and that participants with the COMT genotype polymorphisms would experience a more significant expression of this outcome. This study was a secondary analysis of the Minnesota Green Tea Trial, a randomized placebo-controlled, double-blinded trial investigating the effects of GTE in women who were generally healthy and postmenopausal. The treatment group consumed 843 mg of epigallocatechin gallate daily for 12 months versus placebo. Participants in this study had a mean age of 60 years, were predominantly White, and most had a healthy body mass index. GTE supplementation did not significantly change plasma F2-isoprostanes concentrations compared with placebo after 12 months (P for overall treatment = .07). There were no significant interactions between treatment and age, or body mass index, physical activity, smoking history, and alcohol intake. COMT genotype did not modify the effect of GTE supplementation on F2-isoprostanes concentrations in the treatment group (P = .85). Among participants in the Minnesota Green Tea Trial, consuming GTE supplements daily for 1 year did not result in a significant decrease in plasma F2-isoprostanes concentrations. Likewise, the COMT genotype did not modify the effect of GTE supplementation on F2-isoprostanes concentrations.
KW - COMT genotype
KW - Catechol-O-methyltransferase
KW - F-isoprostanes
KW - Green tea extract
KW - Postmenopause
KW - Women
UR - https://www.scopus.com/pages/publications/85151237425
UR - https://www.scopus.com/pages/publications/85151237425#tab=citedBy
U2 - 10.1016/j.nutres.2023.03.001
DO - 10.1016/j.nutres.2023.03.001
M3 - Article
C2 - 37011435
AN - SCOPUS:85151237425
SN - 0271-5317
VL - 113
SP - 29
EP - 38
JO - Nutrition Research
JF - Nutrition Research
ER -