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      Efficacy of Isomaltulose Compared to Sucrose in Modulating Endothelial Function in Overweight Adults

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          Abstract

          Hyperglycemia is linked to impaired arterial endothelial function (EF), an early sign of cardiovascular disease. We compared the efficacy of low-glycemic index isomaltulose (Palatinose™) with that of sucrose in modulating EF, as assessed by flow-mediated dilation (FMD). In this double-blinded cross-over study, 80 overweight mildly hypertensive subjects were randomized to receive 50 g of either isomaltulose or sucrose. On two non-consecutive days, brachial artery ultrasound FMD scans were obtained prior to and hourly (T0–T3) after carbohydrate load. Blood was drawn immediately after scanning. Glucose and insulin levels were analyzed. Overall, the FMD decrease was attenuated by isomaltulose compared to sucrose (ΔFMD = −0.003% and −0.151%; p > 0.05 for the interaction treatment x period). At T2, FMD was significantly higher after isomaltulose administration compared to that after sucrose administration (FMD = 5.9 ± 2.9% and 5.4 ± 2.6%, p = 0.047). Pearson correlations between FMD and blood glucose showed a trend for a negative association at T0 and T2 independently of the carbohydrate (r-range = −0.20 to −0.23, p < 0.1). Sub-analysis suggested a lower FMD in insulin-resistant (IR) compared to insulin-sensitive subjects. Isomaltulose attenuated the postprandial decline of FMD, particularly in IR persons. These data support the potential of isomaltulose to preserve the endothelial function postprandially and consequently play a favorable role in cardiovascular health.

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          A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women.

          Little is known about the effects of the amount and type of carbohydrates on risk of coronary heart disease (CHD). The objective of this study was to prospectively evaluate the relations of the amount and type of carbohydrates with risk of CHD. A cohort of 75521 women aged 38-63 y with no previous diagnosis of diabetes mellitus, myocardial infarction, angina, stroke, or other cardiovascular diseases in 1984 was followed for 10 y. Each participant's dietary glycemic load was calculated as a function of glycemic index, carbohydrate content, and frequency of intake of individual foods reported on a validated food-frequency questionnaire at baseline. All dietary variables were updated in 1986 and 1990. During 10 y of follow-up (729472 person-years), 761 cases of CHD (208 fatal and 553 nonfatal) were documented. Dietary glycemic load was directly associated with risk of CHD after adjustment for age, smoking status, total energy intake, and other coronary disease risk factors. The relative risks from the lowest to highest quintiles of glycemic load were 1.00, 1.01, 1. 25, 1.51, and 1.98 (95% CI: 1.41, 2.77 for the highest quintile; P for trend /= 23. These epidemiologic data suggest that a high dietary glycemic load from refined carbohydrates increases the risk of CHD, independent of known coronary disease risk factors.
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            The pathophysiology of hypertension in patients with obesity.

            The combination of obesity and hypertension is associated with high morbidity and mortality because it leads to cardiovascular and kidney disease. Potential mechanisms linking obesity to hypertension include dietary factors, metabolic, endothelial and vascular dysfunction, neuroendocrine imbalances, sodium retention, glomerular hyperfiltration, proteinuria, and maladaptive immune and inflammatory responses. Visceral adipose tissue also becomes resistant to insulin and leptin and is the site of altered secretion of molecules and hormones such as adiponectin, leptin, resistin, TNF and IL-6, which exacerbate obesity-associated cardiovascular disease. Accumulating evidence also suggests that the gut microbiome is important for modulating these mechanisms. Uric acid and altered incretin or dipeptidyl peptidase 4 activity further contribute to the development of hypertension in obesity. The pathophysiology of obesity-related hypertension is especially relevant to premenopausal women with obesity and type 2 diabetes mellitus who are at high risk of developing arterial stiffness and endothelial dysfunction. In this Review we discuss the relationship between obesity and hypertension with special emphasis on potential mechanisms and therapeutic targeting that might be used in a clinical setting.
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              Postprandial hyperglycemia/hyperlipidemia (postprandial dysmetabolism) is a cardiovascular risk factor.

              Epidemiologic data indicate that a postprandial state characterized by abnormally increased levels of glucose and lipids (also referred to as postprandial dysmetabolism) is an independent predictor of future cardiovascular events, even in nondiabetic subjects. The cardiovascular toxicity of postprandial dysmetabolism is mediated by oxidant stress, which is directly proportional to the increase in glucose after a meal. This transient increase in free radicals acutely triggers inflammation, endothelial dysfunction, hypercoagulability, sympathetic hyperactivity, and a cascade of other atherogenic changes. The postprandial dysmetabolism hypothesis has been bolstered by interventional studies that have demonstrated that blunting the postprandial spikes in glucose and lipids improves inflammation and endothelial function immediately. Early randomized controlled trials indicate that reducing postprandial dysmetabolism appears to significantly slow atherosclerotic progression and may improve cardiovascular prognosis. In conclusion, postprandial dysmetabolism appears to be an important proximate cause of adverse cardiovascular events. Addressing this fundamental and largely unrecognized condition will require specific screening and treatment strategies. Diet, exercise, and various pharmacologic agents can improve postprandial dysmetabolism. Using these strategies may help improve the prognosis for patients with diabetes mellitus and/or coronary heart disease.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                03 January 2020
                January 2020
                : 12
                : 1
                : 141
                Affiliations
                [1 ]Imagelabonline & Cardiovascular, 4117 GV Erichem, The Netherlands
                [2 ]Amsterdam UMC—Location Academic Medical Centre, Departments of Clinical Epidemiology, Biostatistics and Bioinformatics, and Gastroenterology, 1105 AZ Amsterdam, The Netherlands
                [3 ]BENEO-Institute, c/o BENEO GmbH, Wormser Straße 11, 67283 Obrigheim, Pfalz, Germany; lisa.schweitzer@ 123456beneo.com (L.S.); stephan.theis@ 123456beneo.com (S.T.)
                Author notes
                [* ]Correspondence: ericdg@ 123456xs4all.nl ; Tel.: +31-6-2006-2662
                Author information
                https://orcid.org/0000-0002-5627-855X
                Article
                nutrients-12-00141
                10.3390/nu12010141
                7019610
                31947853
                f712240a-0c79-4d6a-b22f-5f6dd9461f64
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 11 October 2019
                : 31 December 2019
                Categories
                Article

                Nutrition & Dietetics
                isomaltulose,endothelial function,glycemic index,carbohydrates,insulin resistance,cardiovascular health

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