Abstract
ScopeChocolate consumption lowers cardiovascular disease risk, which might be attributed to the methylxanthine theobromine. These effects may be mediated through effects on HDL‐mediated cholesterol efflux, which may be affected by microRNA (miRNA) levels in the HDL particles. Therefore, the aim of this study is to investigate effects of theobromine consumption on fasting and postprandial cholesterol efflux and miRNAs levels.Methods and resultsThirty overweight and 14 obese healthy men and women participated in this randomized, double‐blind crossover study. Participants consumed 500 mg d−1 of theobromine or placebo for 4 weeks. ABCA1‐mediated cholesterol efflux was measured using J774 macrophages. MiRNAs levels (miR‐92a, miR‐223, miR‐135a*) were quantified in apolipoprotein B‐depleted serum. Theobromine consumption did not affect fasting and postprandial cholesterol efflux. Fasting miR‐223 and miR‐135a levels were unchanged, while miR‐92a levels were decreased (−0.21; p < 0.05). The high‐fat meal increased postprandial cholesterol efflux capacity (+4.3 percentage points; p ≤ 0.001), miR‐92a (+1.21; p < 0.001), and miR‐223 (+1.79; p < 0.001) levels, while a trend was found for miR‐135a (+1.08; p = 0.06).ConclusionTheobromine did not improve fasting and postprandial ABCA1‐mediated cholesterol efflux capacity, but decreased fasting miR‐92a levels. High‐fat meal intake increased postprandial cholesterol efflux and the three selected miRNAs levels.
Highlights
223 has previously been reported to indirectly increase cholesterol efflux, the main anti-atherogenicMicroRNAs are small, non-coding RNAs composed effect of HDL.[7]
Four weeks theobromine supplementation did not affect fasting cholesterol efflux capacity (+0.4 percentage point; 95% CI: −2.81, 3.57; p = 0.81), but significantly increased HDL-C concentrations (+0.04 mmol L−1; 95% CI: 0.003, 0.07; p < 0.05)
The test meal did not affect HDL-C concentrations in both conditions, that is, without (+0.01 mmol L−1; 95% CI: −0.01, 0.03; p = 0.16) or with theobromine; (+0.003 mmol L−1; 95% CI: −0.01, 0.02; p = 0.69), During the control period, apoA1 concentrations (+0.02 g L−1; 95% CI: 0.004, 0.05; 1800027 (3 of 8)
Summary
223 has previously been reported to indirectly increase cholesterol efflux, the main anti-atherogenic. MicroRNAs (miRNA) are small, non-coding RNAs composed effect of HDL.[7] Whether miR-135a and miR-92a are related of about 22 nucleotides that bind to complementary sites in to cholesterol efflux has never been studied. Not much is known about the effects of diet on HDL-mediated. J. Plat Department of Nutrition and Movement Sciences NUTRIM School of Nutrition and Translational Research in Metabolism cholesterol efflux and miRNAs concentrations, which may provide explanations for observed associations between diet or dietary components with CVD risk. For example, is associated with a reduction in the risk to de-
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