Endothelial Function in Overweight Adult

Nutrients 2020 , 12 , 141

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decline in postprandial FMD at T1 and T2 for both IR and IS subjects (paired t test; p > 0.05). At T3, the consumption of isomaltulose resulted in an FMD which was comparable to baseline FMD for both IS and IR subjects. In contrast, the consumption of sucrose showed an increase in FMD exceeding the baseline value. Table 2. Change in flow ‐ mediated dilation from baseline in the subjects classified as insulin ‐ sensitive and insulin ‐ resistant according to HOMA index 1,2 . FMD Change from Baseline (T0, %) Time Points Insulin Sensitivity Isomaltulose p Value 3 Sucrose p Value 3 ∆ FMD T1 ‐ T0 IS − 0.16 ± 2.02 0.285 − 0.74 ± 1.92 0.107 IR − 0.81 ± 1.96 − 1.74 ± 2.54 ∆ FMD T2 ‐ T0 IS 0.34 ± 2.33 0.180 − 0.23 ± 1.92 0.435 IR − 0.62 ± 2.35 − 0.68 ± 2.17 ∆ FMD T3 ‐ T0 IS 0.12 ± 2.36 0.794 0.65 ± 2.10 0.692 IR − 0.07 ± 2.54 0.40 ± 2.35 1 FMD, flow ‐ mediated dilation; HOMA, homeostasis model assessment; IR, insulin resistant (HOMA ≥ 2.5); IS, insulin sensitive (HOMA < 2.5). 2 Values are reported as mean ± SD. 3 No significant differences between IR and IS subjects; unpaired t test: p > 0.05. 4. Discussion We hypothesized that the decrease in endothelial function caused by food intake could be attenuated by low ‐ GI foods compared to high ‐ GI carbohydrates. The assumption was tested in mildly hypertensive overweight/obese adults using either sucrose (GI = 65) or isomaltulose (GI = 32). As a novel key finding, our data revealed a preservation of postprandial FMD following the intake of isomaltulose compared to sucrose. Consequently, our results support the hypothesis. The exploratory analysis showed that after two hours, endothelium ‐ dependent vasodilation was significantly higher for isomaltulose ingestion compared to sucrose ingestion (FMD = 5.9 ± 2.9% vs. 5.4 ± 2.6%; paired t test: p < 0.05, Error! Reference source not found. Figure 2A). This finding is in accordance with the literature [20,21]. Lavi et al. investigated the postprandial effects of foods varying in their GI on EF [21]. The higher decrease in FMD after ingestion of high ‐ GI foods found by the authors was confirmed by another intervention study testing different types of rice [20]. Our present study also addresses more general issues regarding high ‐ GI food intake and its physiological consequences. In particular, there is increasing evidence suggesting an association between the GI of foods and CVD [20,25,36,37]. In that context, it is known that postprandial hyperglycemia induces oxidative stress, triggering atherogenic alterations, like secretion of pro ‐ inflammatory cytokines, adhesion molecules, or vasoconstrictive substances (e.g., endothelin ‐ 1) [14,38,39]. Consecutive atherogenic alterations contribute to cell damage, including to cells of the vascular endothelium, and when recurring, resulting in ED [16,18,40]. Moreover, ED was observed to be improved through the administration of antioxidants in vitro [41] and in vivo [42]. Previous studies confirmed a lower blood glucose response in the early postprandial state followed by a more sustained glucose response in the later postprandial state with isomaltulose ingestion when compared with ingestion of rapidly absorbable carbohydrates [43,44]. By preventing hyperglycemia, isomaltulose may have less impact on EF and, hence, could be beneficial also for cardiovascular health. In the current study, we did not observe a lower blood glucose response with isomaltulose, which can be attributed to the restrictive blood sampling time points (i.e., only after 1, 2, and 3 h). Rather, the later postprandial state was examined, and early postprandial glucose peaks were probably missed. This is supported by previous studies showing a rapid blood glucose decrease with sucrose ingestion already before and around 60 min [44]. A second explanation for the link between the GI of foods and CVD involves the action of insulin. Because insulin is a vasodilatory agent, insulin resistance might impair EF. Insulin signaling is important for vasodilation through the activation of endothelial NO synthase. Hence, insulin

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