Acute effects of an oral supplement of (-)-epicatechin on postprandial fat and carbohydrate metabolism in normal and overweight subjects

Abstract

Postprandial hyperglycemia, in particular when accompanied by excessive hypertriglyceridemia, is associated with increased cardiovascular risk, mainly in overweight or obese subjects, as it favors oxidative stress, systemic inflammation and endothelial dysfunction. Thus, treatments that favorably modulate metabolism by reducing steep increases in postprandial serum glucose and triglycerides, are of considerable interest. Evidence suggests that (-)-epicatechin (EPI) is responsible for reductions in cardiometabolic risk associated with chocolate consumption; these effects may be associated with favorable effects of EPI on postprandial metabolism. The aims of this study were to assess the effects of EPI on postprandial metabolism in normal-weight and overweight/obese subjects. Twenty adult volunteers (normal and overweight) underwent oral metabolic tolerance tests in the absence and presence of oral EPI (1 mg kg(-1)). Metabolic responses were examined using indirect calorimetry and determining blood glucose and triglycerides at 0, 2 and 4 hours after metabolic load ingestion. Results show that EPI increased postprandial lipid catabolism, as evidenced by a significant decrease in the respiratory quotient, which implies an increase in fat oxidation. The effect was associated with significantly lower postprandial plasma glucose and triglycerides concentrations. The effects were more prominent in overweight subjects. In conclusion, EPI modulates postprandial metabolism by enhancing lipid oxidation accompanied by reductions in glycemia and triglyceridemia.

Figures

Figure 1

Respiratory coefficient chart and theoretical curve switch in metabolism meal ingestion. The respiratory coefficients usually vary from 1.0 (representing the value expected for pure carbohydrate oxidation) to ~0.7 (the value expected for pure fat oxidation).

Figure 2

Respiratory quotient values and estimated percent kilocalories obtained from fat oxidation in (A, C) normal (n=12) and (B, D) overweight (n=8) subjects, recorded at 0, 2 and 4 hours during the OMTT. Data are expressed as mean ± SD, p values by paired t-tests, where *p <0.05. As seen, the postprandial increase in RQ was significantly attenuated and lipid catabolism was enhanced by EPI in both groups.

Figure 3

Comparison of percent change in lipid oxidation, at 2 hours after meal ingestion (vs. fasting state) between (A) normal (n=12) and (B) overweight (n=8) subjects. Non-parametric analyses were performed to compare differences between means. Postprandial fat oxidation in overweight subjects decreased more than among the normal subjects in the absence of EPI. However, with EPI supplementation such decrease was blunted.

Figure 4

Comparison of lipid oxidation between normal and high body fat subjects, 2 hours after meal ingestion. Lipid oxidation was significantly increased in high body fat subjects. Data are expressed as mean ± SD, p values by paired t-tests.

Figure 5

Comparison of glycemia between normal and high adiposity subjects, 2 hours after meal ingestion. Glycemia was significantly attenuated in high adiposity subjects. Data are expressed as mean ± SD, p values by paired t-tests.

Figure 6

Comparison of triglyceridemia between normal and high body fat subjects, 2 hours after meal ingestion. Triglyceridemia was attenuated in high adiposity subjects. Data are expressed as mean ± SD, p values by paired t-tests.