Nutrients 2020 , 12 , 141
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not yet completely understood, a key vasodilator is known to be nitric oxide (NO). A decline in NO synthesis, through the inhibition of, e.g., NO synthase, leads to an impaired vasodilation of blood vessels [8], which contributes to hypertension and promotes the clinical symptoms of CVD. Besides a reduced NO bioavailability, ED is characterized by oxidative stress and an increase of inflammatory as well as thrombotic factors [9]. Furthermore, it is well known that clinical states of insulin resistance, including obesity, metabolic syndrome, and diabetes mellitus, are associated with impaired endothelium ‐ dependent vasodilation [9,10]. This can be explained by the vasodilatory properties of insulin, mediating NO synthesis via its stimulation of the insulin receptor and, finally, increasing NO bioavailability in healthy humans [8]. In contrast, in insulin ‐ resistant persons, insulin signaling is impaired not only at the metabolic but also at the vascular level [11], and moreover, the concentration of the vasoconstrictor endothelin ‐ 1 was found to be increased [10]. Thus, insulin resistance is accompanied by an increased risk for ED [9]. Besides insulin resistance itself, accumulating evidence indicates a link between EF and postprandial dysmetabolism such as hyperglycemia and its consequences, i.e., vascular events [12– 14]. Hyperglycemia is postulated to induce oxidative stress and impair EF [15], which is in accordance with the FMD decline occurring directly after food intake [16–19]. There is some evidence that low ‐ glycemic index (GI) foods may favorably influence EF [20,21]. This was firstly examined by Lavi et al., who investigated differences in postprandial FMD in response to foods with various glycemic indices [21]. The authors found a significant decrease in FMD compared to baseline two hours after food ingestion, which was the highest after glucose ingestion, followed by cornflakes intake. Although a low ‐ GI food (fiber ‐ rich cereals) showed a slight decrease in FMD in the postprandial state as well, the decrease was not significant and comparable with the FMD decrease induced by water [21]. In alignment with the results of Lavi et al., other dietary intervention studies previously showed an improvement in blood pressure or pulse wave velocity due to low ‐ GI compared to high ‐ GI diets [22,23], which would also explain the positive association between glycemic index and CVD [24–26]. The hypothesis that hyperglycemia causes ED is supported by the observation that overweight and obese individuals and those with diabetes, either type 1 or type 2, are more prone to ED [8,11,27,28]. As these persons are at higher risk of postprandial dysmetabolism, continuous exposure to elevated blood glucose induces oxidative stress and chronic inflammation [18,29], both predictors of ED. Moreover, insulin resistance might have additive adverse effects on the vascular function [11]. On the basis of this knowledge and considering the large intake of high ‐ GI foods that characterizes today’s Western diet, low ‐ GI foods might be effective in preventing ED. For instance, a substantial replacement of sugar by low ‐ GI carbohydrates, e.g., isomaltulose (Palatinose™, BENEO GmbH, 68165 Mannheim, Germany), may contribute to improved cardiovascular health, as indicated by Keller et al. [30]. During this study on inactivity in healthy young men, prolonged vascular relaxation, assessed by the augmentation index, was observed after isomaltulose ingestion compared to sucrose administration [30]. Both sucrose and isomaltulose are disaccharides consisting of a glucose and a fructose monomer, which provide the same amount of calories. However, they differ in their glycosidic bond, which is α‐ 1,2 for sucrose and α‐ 1,6 for isomaltulose [31]. The bond present in isomaltulose causes its slower absorption in the small intestine, thus resulting in a low GI (32 for isomaltulose vs. 65 for sucrose) [32,33]. The present exploratory study aimed to investigate the acute effects of isomaltulose versus those of sucrose on endothelium ‐ dependent vasodilation, i.e., FMD, in overweight/obese subjects. The lower blood glucose response following isomaltulose load may allow for enhanced preservation of EF. We therefore hypothesized that, compared to sucrose, isomaltulose would cause lesser postprandial impairment of EF in overweight/obese individuals.
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