Blackcurrants are rich in polyphenolic glycosides called anthocyanins, which may inhibit postprandial glycemia. The aim was to determine the dose-dependent effects of blackcurrant extract on postprandial glycemia. Men and postmenopausal women (14 M, 9 W, mean age 46 years, S.D.=14) were enrolled into a randomized, double-blind, crossover trial. Low sugar fruit drinks containing blackcurrant extract providing 150-mg (L-BE), 300-mg (M-BE) and 600-mg (H-BE) total anthocyanins or no blackcurrant extract (CON) were administered immediately before a high-carbohydrate meal. Plasma glucose, insulin and incretins (GIP and GLP-1) were measured 0–120 min, and plasma 8-isoprostane F2α, together with arterial stiffness by digital volume pulse (DVP) was measured at 0 and 120 min. Early plasma glucose response was significantly reduced following H-BE (n=22), relative to CON, with a mean difference (95% CI) in area over baseline (AOB) 0-30 min of −0.34 mmol/l.h (−0.56, −0.11, P<.005); there were no differences between the intermediate doses and placebo. Plasma insulin concentrations (AOB 0–30 min) were similarly reduced. Plasma GIP concentrations (AOB 0–120 min) were significantly reduced following H-BE, with a mean difference of −46.6 ng/l.h (−66.7, −26.5, P<.0001) compared to CON. Plasma GLP-1 concentrations were reduced following H-BE at 90 min. There were no effects on 8-isoprostane F2α or vascular function. Consumption of blackcurrant extract in amounts roughly equivalent to 100-g blackcurrants reduced postprandial glycemia, insulinemia and incretin secretion, which suggests that inclusion of blackcurrant polyphenols in foods may provide cardio-metabolic health benefits. This trial was registered at clinicaltrials.gov as NCT01706653.
The beneficial effects of green tea catechins, such as the proposed improvement in endothelial function, may be influenced by phase II metabolism during and after absorption. The methylation enzyme, catechol-O-methyltransferase (COMT), has a missense mutation rs4680 (G to A), proposed to result in a 40 % reduction in enzyme activity. In the present pilot study, twenty subjects (ten of each homozygous COMT genotype) were recruited. Green tea extract capsules (836 mg green tea catechins) were given in a fasted state, and a high-carbohydrate breakfast was given after 60 min. Blood samples and vascular function measurements were taken at regular intervals. The change in digital volume pulse stiffness index (SI) from baseline was shown to be different between genotype groups at 120 and 240 min, with a lower SI in the GG individuals (P# 0·044). The change in blood pressure from baseline also differed between genotype groups, with a greater increase in systolic (P¼ 0·023) and diastolic (P¼ 0·034) blood pressure at 120 min in the GG group. The AA group was shown to have a greater increase in insulin concentrations at 120 min (P¼ 0·019) and 180 min (P¼ 0·008) compared with baseline, despite similar glucose profiles. No genotypic differences were found in vascular reactivity measured using laser Doppler iontophoresis, total nitrite, lipids, plasma total antioxidant capacity or inflammatory markers after ingestion of the green tea extract. In conclusion, SI and insulin response to the glucose load differed between the COMT genotype groups, and this may be suggestive of a green tea extract and genotype interaction. Green tea contains high levels of polyphenols (approximately 70 % of dry weight), which are mainly green tea catechins belonging to the flavan-3-ol family of polyphenols. Of highest abundance is epigallocatechin gallate, followed by epigallocatechin, epicatechin and epicatechin gallate. Epidemiological studies have repeatedly observed a beneficial effect of green tea consumption on the risk of CVD (1 -5) . In addition, acute and chronic human intervention studies have demonstrated benefits of green tea and its constituent catechins on vascular function and reactivity (6 -9) . Proposed molecular mechanisms for improved vascular reactivity include increased endothelial NO synthase activity (10) , reduced cytokine (11,12) and prooxidant production (13) and NADPH oxidase inhibition (14) .Flavan-3-ol O-methylation is a major pathway of flavonoid metabolism, which mainly occurs in the intestinal tract, liver and kidney. This phase II metabolism is thought to reduce the biological activity of flavan-3-ol polyphenols. Indeed, variability in flavonoid O-methylation has been shown to influence the effect of dietary flavonoids on endothelial function (15) . O-Methylation of flavonoids is catalysed by the enzyme catechol-O-methyltransferase (COMT). A common genetic missense mutation (G to A base change) results in a valine-to-methionine amino acid substitution at position 108 in the soluble protein and at position ...
In conclusion, the COMT Val(158/108)Met does not appear to have a dramatic influence on EGCG absorption and elimination. However, further pharmacokinetic research is needed to substantiate these findings.
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