Why the study?
Resveratrol has shown promising anti-inflammatory effects in in vitro and animal studies, but its effect on arterial inflammation in vivo needed investigation.
Does resveratrol reduce arterial and systemic inflammation in males at risk of type 2 diabetes?
Does resveratrol reduce arterial and systemic inflammation in males at risk of type 2 diabetes?
In a small crossover trial of men at risk for type 2 diabetes, resveratrol 150 mg/day for 34 days failed to attenuate arterial or systemic inflammation as measured by 18F-FDG PET/CT.
Resveratrol does not reduce arterial inflammation on PET/CT; challenges preclinical data and leaves open questions for larger human trials.
Purpose Resveratrol has shown promising anti-inflammatory effects in in vitro and animal studies. We aimed to investigate this effect on arterial inflammation in vivo. Methods This was an additional analysis of a double-blind randomized crossover trial which included eight male subjects with decreased insulin sensitivity who underwent an 18F-fluoroxyglucose (18F-FDG) PET/CT after 34 days of placebo and resveratrol treatment (150 mg/day). 18F-FDG uptake was analyzed in the carotid arteries and the aorta, adipose tissue regions, spleen, and bone marrow as measures for arterial and systemic inflammation. Maximum target-to-background ratios (TBRmax) were compared between resveratrol and placebo treatment with the non-parametric Wilcoxon signed-rank test. Median values are shown with their interquartile range. Results Arterial 18F-FDG uptake was non-significantly higher after resveratrol treatment (TBRmax all vessels 1.7 (1.6–1.7)) in comparison to placebo treatment (1.5 (1.4–1.6); p=0.050). Only in visceral adipose tissue, the increase in 18F-FDG uptake after resveratrol reached statistical significance (p=0.024). Furthermore, CRP-levels were not significantly affected by resveratrol treatment (p=0.091). Conclusions Resveratrol failed to attenuate arterial or systemic inflammation as measured with 18F-FDG PET in subjects at risk of developing type 2 diabetes. However, validation of these findings in larger human studies is needed.
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Boswijk et al. (2021) studied this question.
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