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Dietary Supplementation and Vascular Function

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (10 December 2019) | Viewed by 40980

Special Issue Editor


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Guest Editor
Department of Nutrition, Food & Exercise Sciences, College of Human Sciences, Florida State University, 242N Sandels Building l, 120 Convocation Way, Tallahassee, FL 32306-1490, USA
Interests: The impact of exercise and nutrition on the regulation of blood flow and metabolism in skeletal muscle and adipose tissue to improve cardiometabolic disease risk across the lifespan

Special Issue Information

Dear Colleagues,

The purpose of this Special Issue “Dietary Supplementation and Vascular Function” is to provide an overview of relevant nutritional interventions that impact vascular function. Nutraceutical and dietary supplement industries have ever-expanding markets. The goal of this Special Issue is to provide evidence regarding the effectiveness, or ineffectiveness, of supplements to improve vascular function. The relative effectiveness is likely dependent on the specifics of the nutrient with respect to dose and conditions of intake, as well as the individuals studied: sedentary or physically active, young or older, healthy or in a diseased state. In this Special Issue, we would like to take a closer look at the effects of nutrients on vascular function. A short list of such nutrients follows.

  • Creatine
  • Isoflavones
  • Macronutrients
  • Nitrates
  • Vitamin D

Prof. Dr. Robert C. Hickner
Guest Editor

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Keywords

  • Dietary supplementation
  • Endothelial dysfunction
  • Exercise
  • Nitric oxide
  • Nutrition
  • Obesity
  • Vascular disease

Published Papers (6 papers)

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Research

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18 pages, 3536 KiB  
Article
Beneficial Effect of a Multistrain Synbiotic Prodefen® Plus on the Systemic and Vascular Alterations Associated with Metabolic Syndrome in Rats: The Role of the Neuronal Nitric Oxide Synthase and Protein Kinase A
by Pablo Llévenes, Raquel Rodrigues-Díez, Laia Cros-Brunsó, Mᵃ Isabel Prieto, Laura Casaní, Gloria Balfagón and Javier Blanco-Rivero
Nutrients 2020, 12(1), 117; https://doi.org/10.3390/nu12010117 - 1 Jan 2020
Cited by 13 | Viewed by 4297
Abstract
A high fat diet (HFD) intake is crucial for the development and progression of metabolic syndrome (MtS). Increasing evidence links gut dysbiosis with the metabolic and vascular alterations associated with MtS. Here we studied the use of a combination of various probiotic strains [...] Read more.
A high fat diet (HFD) intake is crucial for the development and progression of metabolic syndrome (MtS). Increasing evidence links gut dysbiosis with the metabolic and vascular alterations associated with MtS. Here we studied the use of a combination of various probiotic strains together with a prebiotic (synbiotic) in a commercially available Prodefen® Plus. MtS was induced by HFD (45%) in male Wistar rats. Half of the MtS animals received Prodefen® Plus for 4 weeks. At 12 weeks, we observed an increase in body weight, together with the presence of insulin resistance, liver steatosis, hypertriglyceridemia and hypertension in MtS rats. Prodefen® Plus supplementation did not affect the body weight gain but ameliorated all the MtS-related symptoms. Moreover, the hypertension induced by HFD is caused by a diminished both nitric oxide (NO) functional role and release probably due to a diminished neuronal nitric oxide synthase (nNOS) activation by protein kinase A (PKA) pathway. Prodefen® Plus supplementation for 4 weeks recovered the NO function and release and the systolic blood pressure was returned to normotensive values as a result. Overall, supplementation with Prodefen® Plus could be considered an interesting non-pharmacological approach in MtS. Full article
(This article belongs to the Special Issue Dietary Supplementation and Vascular Function)
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15 pages, 273 KiB  
Communication
Pharmacological and Nutritional Modulation of Vascular Calcification
by Liv M. Vossen, Abraham A. Kroon, Leon J. Schurgers and Peter W. de Leeuw
Nutrients 2020, 12(1), 100; https://doi.org/10.3390/nu12010100 - 30 Dec 2019
Cited by 27 | Viewed by 5777
Abstract
Vascular calcification is an independent predictor of cardiovascular disease, and therefore, inhibition or regression of this processes is of clinical importance. The standard care regarding prevention and treatment of cardiovascular disease at this moment mainly depends on drug therapy. In animal and preclinical [...] Read more.
Vascular calcification is an independent predictor of cardiovascular disease, and therefore, inhibition or regression of this processes is of clinical importance. The standard care regarding prevention and treatment of cardiovascular disease at this moment mainly depends on drug therapy. In animal and preclinical studies, various forms of cardiovascular drug therapy seem to have a positive effect on vascular calcification. In particular, calcium channel blockers and inhibitors of the renin–angiotensin–aldosteron system slowed down arterial calcification in experimental animals. In humans, the results of trials with these drugs are far less pronounced and often contradictory. There is limited evidence that the development of new atherosclerotic lesions may be retarded in patients with coronary artery disease, but existing lesions can hardly be influenced. Although statin therapy has a proven role in the prevention and treatment of cardiovascular morbidity and mortality, it is associated with both regression and acceleration of the vascular calcification process. Recently, nutritional supplements have been recognized as a potential tool to reduce calcification. This is particularly true for vitamin K, which acts as an inhibitor of vascular calcification. In addition to vitamin K, other dietary supplements may also modulate vascular function. In this narrative review, we discuss the current state of knowledge regarding the pharmacological and nutritional possibilities to prevent the development and progression of vascular calcification. Full article
(This article belongs to the Special Issue Dietary Supplementation and Vascular Function)
11 pages, 1435 KiB  
Article
Orexin-A Exerts Equivocal Role in Atherosclerosis Process Depending on the Duration of Exposure: In Vitro Study
by Narjes Nasiri Ansari, Flora Spentza, Georgios K. Dimitriadis, Aphrodite Daskalopoulou, Angeliki Karapanagioti, Gerasimos Siasos, Evi Lianidou, Athanasios G. Papavassiliou, Eva Kassi and Harpal S. Randeva
Nutrients 2020, 12(1), 53; https://doi.org/10.3390/nu12010053 - 24 Dec 2019
Cited by 1 | Viewed by 2587
Abstract
Orexin-A is a peptide hormone that plays a crucial role in feeding regulation and energy homeostasis. Diurnal intermittent fasting (DIF) has been found to increase orexin-A plasma levels during fasting hours, while Ramadan fasting which resembles DIF, has led to beneficial effects on [...] Read more.
Orexin-A is a peptide hormone that plays a crucial role in feeding regulation and energy homeostasis. Diurnal intermittent fasting (DIF) has been found to increase orexin-A plasma levels during fasting hours, while Ramadan fasting which resembles DIF, has led to beneficial effects on endothelial function. Herein, we aimed to investigate the effects of orexin-A on the expression of molecules involved in the atherogenesis process: Monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9) and tissue inhibitor of metalloproteinase-1 and 2 (TIMP-1 and TIMP-2), in human aortic endothelial cells (HAECs). HAECs were incubated with orexin-A at concentrations of 40 ng/mL, 200 ng/mL and 400 ng/mL for 6, 12 and 24 h. The mRNA levels of MCP-1, MMP-2, MMP-9, TIMP-1, and TIMP-2 and orexin-1 receptor were measured by real-time qPCR. We also evaluated the MMP-2, p38, phospho-p38, NF-κΒ/p65 as well as TIMP-1 protein levels by Western blot and ELISA, respectively. MMP-2 activity was measured by gelatin zymography. Short-term 6-h incubation of HAECs with orexin-A at a high concentration (400 ng/mL) decreased MCP-1, MMP-2 expression, MMP-2/TIMP-1 ratio (p < 0.05), and MMP-2 activity, while incubation for 24 h increased MCP-1, MMP-2 expression (p < 0.05), MMP-2/TIMP-1 and MMP-2/TIMP-2 ratio (p < 0.01 and p < 0.05, respectively) as well as MMP-2 activity. The dual effects of orexin-A are mediated, at least in part, via regulation of p38 and NF-κΒ pathway. Orexin-A may have an equivocal role in atherosclerosis process with its effects depending on the duration of exposure. Full article
(This article belongs to the Special Issue Dietary Supplementation and Vascular Function)
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14 pages, 716 KiB  
Article
Microencapsulated Pomegranate Reverts High-Density Lipoprotein (HDL)-Induced Endothelial Dysfunction and Reduces Postprandial Triglyceridemia in Women with Acute Coronary Syndrome
by Diego Estrada-Luna, Elizabeth Carreón-Torres, Rocío Bautista-Pérez, Gabriel Betanzos-Cabrera, Alan Dorantes-Morales, María Luna-Luna, Jesús Vargas-Barrón, Ana María Mejía, José Manuel Fragoso, Karla Carvajal-Aguilera, José J. García-Trejo, Gilberto Vargas-Alarcón and Óscar Pérez-Méndez
Nutrients 2019, 11(8), 1710; https://doi.org/10.3390/nu11081710 - 25 Jul 2019
Cited by 15 | Viewed by 3356
Abstract
(1) Background: the composition of high-density lipoproteins (HDL) becomes altered during the postprandial state, probably affecting their functionality vis-à-vis the endothelium. Since acute coronary syndrome (ACS) in women is frequently associated with endothelial dysfunction, it is likely that HDL are unable to improve [...] Read more.
(1) Background: the composition of high-density lipoproteins (HDL) becomes altered during the postprandial state, probably affecting their functionality vis-à-vis the endothelium. Since acute coronary syndrome (ACS) in women is frequently associated with endothelial dysfunction, it is likely that HDL are unable to improve artery vasodilation in these patients. Therefore, we characterized HDL from women with ACS in fasting and postprandial conditions. We also determined whether microencapsulated pomegranate (MiPo) reverts the HDL abnormalities, since previous studies have suggested that this fruit improves HDL functionality. (2) Methods: Eleven women with a history of ACS were supplemented daily with 20 g of MiPo, for 30 days. Plasma samples were obtained during fasting and at different times, after a lipid load test to determine the lipid profile and paraoxonase–1 (PON1) activity. HDL were isolated by sequential ultracentrifugation to determine their size distribution and to assess their effect on endothelial function, by using an in vitro model of rat aorta rings. (3) Results: MiPo improved the lipid profile and increased PON1 activity, as previously reported, with fresh pomegranate juice. After supplementation with MiPo, the incremental area under the curve of triglycerides decreased to half of the initial values. The HDL distribution shifted from large HDL to intermediate and small-size particles during the postprandial period in the basal conditions, whereas such a shift was no longer observed after MiPo supplementation. Consistently, HDL isolated from postprandial plasma samples hindered the vasodilation of aorta rings, and this endothelial dysfunction was reverted after MiPo consumption. (4) Conclusions: MiPo exhibited the same beneficial effects on the lipid profile and PON1 activity as the previously reported fresh pomegranate. In addition, MiPo supplementation reverted the negative effects of HDL on endothelial function generated during the postprandial period in women with ACS. Full article
(This article belongs to the Special Issue Dietary Supplementation and Vascular Function)
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Review

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17 pages, 1210 KiB  
Review
Vitamin D and Endothelial Function
by Do-Houn Kim, Cesar A. Meza, Holly Clarke, Jeong-Su Kim and Robert C. Hickner
Nutrients 2020, 12(2), 575; https://doi.org/10.3390/nu12020575 - 22 Feb 2020
Cited by 180 | Viewed by 18188
Abstract
Vitamin D is known to elicit a vasoprotective effect, while vitamin D deficiency is a risk factor for endothelial dysfunction (ED). ED is characterized by reduced bioavailability of a potent endothelium-dependent vasodilator, nitric oxide (NO), and is an early event in the development [...] Read more.
Vitamin D is known to elicit a vasoprotective effect, while vitamin D deficiency is a risk factor for endothelial dysfunction (ED). ED is characterized by reduced bioavailability of a potent endothelium-dependent vasodilator, nitric oxide (NO), and is an early event in the development of atherosclerosis. In endothelial cells, vitamin D regulates NO synthesis by mediating the activity of the endothelial NO synthase (eNOS). Under pathogenic conditions, the oxidative stress caused by excessive production of reactive oxygen species (ROS) facilitates NO degradation and suppresses NO synthesis, consequently reducing NO bioavailability. Vitamin D, however, counteracts the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase which produces ROS, and improves antioxidant capacity by enhancing the activity of antioxidative enzymes such as superoxide dismutase. In addition to ROS, proinflammatory mediators such as TNF-α and IL-6 are risk factors for ED, restraining NO and eNOS bioactivity and upregulating the expression of various atherosclerotic factors through the NF-κB pathway. These proinflammatory activities are inhibited by vitamin D by suppressing NF-κB signaling and production of proinflammatory cytokines. In this review, we discuss the diverse activities of vitamin D in regulating NO bioavailability and endothelial function. Full article
(This article belongs to the Special Issue Dietary Supplementation and Vascular Function)
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21 pages, 1139 KiB  
Review
Resveratrol and the Interaction between Gut Microbiota and Arterial Remodelling
by Andy W.C. Man, Huige Li and Ning Xia
Nutrients 2020, 12(1), 119; https://doi.org/10.3390/nu12010119 - 1 Jan 2020
Cited by 19 | Viewed by 6309
Abstract
Arterial remodelling refers to the alteration in the structure of blood vessel that contributes to the progression of hypertension and other cardiovascular complications. Arterial remodelling is orchestrated by the crosstalk between the endothelium and vascular smooth muscle cells (VSMC). Vascular inflammation participates in [...] Read more.
Arterial remodelling refers to the alteration in the structure of blood vessel that contributes to the progression of hypertension and other cardiovascular complications. Arterial remodelling is orchestrated by the crosstalk between the endothelium and vascular smooth muscle cells (VSMC). Vascular inflammation participates in arterial remodelling. Resveratrol is a natural polyphenol that possesses anti-oxidant and anti-inflammatory properties and has beneficial effects in both the endothelium and VSMC. Resveratrol has been studied for the protective effects in arterial remodelling and gut microbiota, respectively. Gut microbiota plays a critical role in the immune system and inflammatory processes. Gut microbiota may also regulate vascular remodelling in cardiovascular complications via affecting endothelium function and VSMC proliferation. Currently, there is new evidence showing that gut microbiota regulate the proliferation of VSMC and the formation of neointimal hyperplasia in response to injury. The change in population of the gut microbiota, as well as their metabolites (e.g., short-chain fatty acids) could critically contribute to VSMC proliferation, cell cycle progression, and migration. Recent studies have provided strong evidence that correlate the effects of resveratrol in arterial remodelling and gut microbiota. This review aims to summarize recent findings on the resveratrol effects on cardiovascular complications focusing on arterial remodelling and discuss the possible interactions of resveratrol and the gut microbiota that modulate arterial remodelling. Full article
(This article belongs to the Special Issue Dietary Supplementation and Vascular Function)
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