scholarly journals Role of Polyphenols and Carotenoids in Endothelial Dysfunction: An Overview from Classic to Innovative Biomarkers

2020 ◽  
Vol 2020 ◽  
pp. 1-19
Author(s):  
Natalia Di Pietro ◽  
Maria Pompea Antonia Baldassarre ◽  
Angelo Cichelli ◽  
Assunta Pandolfi ◽  
Gloria Formoso ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Metabolic Diseases ◽  
Complementary Therapy ◽  
Platelet Activity ◽  
Main Challenge ◽  
Obesity And Diabetes ◽  
Dietary Nutrients ◽  
Health Promoting

Nowadays, the dramatically increased prevalence of metabolic diseases, such as obesity and diabetes mellitus and their related complications, including endothelial dysfunction and cardiovascular disease, represents one of the leading causes of death worldwide. Dietary nutrients together with healthy lifestyles have a crucial role in the endothelium health-promoting effects. From a growing body of evidence, active natural compounds from food, including polyphenols and carotenoids, have attracted particular attention as a complementary therapy on atherosclerosis and cardiovascular disease, as well as preventive approaches through the attenuation of inflammation and oxidative stress. They mainly act as radical scavengers by promoting a variety of biological mechanisms, such as improvements in endothelial function, blood pressure, platelet activity, and insulin sensitivity, and by modulating various known biomarkers. The present review highlights the role of polyphenols and carotenoids in early endothelial dysfunction with attention to their beneficial effect in modulating both classical and recent technologically generated emerging biomarkers. These, alone or in combination, can play an important role in the prediction, diagnosis, and evolution of cardiovascular disease. However, a main challenge is to speed up early and prompt new interventions in order to prevent or slow down disease progression, even with an adequate intake of bioactive compounds. Hence, there is an urgent need of new more validated, appropriate, and reliable diagnostic and therapeutic biomarkers useful to diagnose endothelial dysfunction at an earlier stage.

scholarly journals Role of Endothelial Dysfunction in Cardiovascular Disease: A Review

2000 ◽  
Vol 5 (2) ◽  
pp. 59-66
Author(s):  
Amudha Kadirvelu ◽  
Chee Kok Han ◽  
Tan Kim Heung ◽  
Anna Maria Choy ◽  
Mustafa Mohd Rais ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction

scholarly journals Platelet regulation of myeloid suppressor of cytokine signaling 3 accelerates atherosclerosis

2019 ◽  
Vol 11 (517) ◽  
pp. eaax0481 ◽  
Author(s):  
Tessa J. Barrett ◽  
Martin Schlegel ◽  
Felix Zhou ◽  
Mike Gorenchtein ◽  
Jennifer Bolstorff ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Cytokine Signaling ◽  
Platelet Activity ◽  
Suppressor Of Cytokine Signaling ◽  
Phagocytic Capacity ◽  
Monocyte Migration ◽  
Socs3 Expression ◽  
Platelet Aggregate ◽  
Inflammatory Phenotype

Platelets are best known as mediators of hemostasis and thrombosis; however, their inflammatory effector properties are increasingly recognized. Atherosclerosis, a chronic vascular inflammatory disease, represents the interplay between lipid deposition in the artery wall and unresolved inflammation. Here, we reveal that platelets induce monocyte migration and recruitment into atherosclerotic plaques, resulting in plaque platelet-macrophage aggregates. In Ldlr−/− mice fed a Western diet, platelet depletion decreased plaque size and necrotic area and attenuated macrophage accumulation. Platelets drive atherogenesis by skewing plaque macrophages to an inflammatory phenotype, increasing myeloid suppressor of cytokine signaling 3 (SOCS3) expression and reducing the Socs1:Socs3 ratio. Platelet-induced Socs3 expression regulates plaque macrophage reprogramming by promoting inflammatory cytokine production (Il6, Il1b, and Tnfa) and impairing phagocytic capacity, dysfunctions that contribute to unresolved inflammation and sustained plaque growth. Translating our data to humans with cardiovascular disease, we found that women with, versus without, myocardial infarction have up-regulation of SOCS3, lower SOCS1:SOCS3, and increased monocyte-platelet aggregate. A second cohort of patients with lower extremity atherosclerosis demonstrated that SOCS3 and the SOCS1:SOCS3 ratio correlated with platelet activity and inflammation. Collectively, these data provide a causative link between platelet-mediated myeloid inflammation and dysfunction, SOCS3, and cardiovascular disease. Our findings define an atherogenic role of platelets and highlight how, in the absence of thrombosis, platelets contribute to inflammation.

scholarly journals Integrated Role of Nutrition and Physical Activity for Lifelong Health

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1437 ◽  
Author(s):  
Karsten Koehler ◽  
Clemens Drenowatz
Keyword(s):  
Physical Activity ◽  
Diabetes Mellitus ◽  
Cardiovascular Disease ◽  
Body Composition ◽  
Metabolic Diseases ◽  
Musculoskeletal Health ◽  
Healthy Nutrition ◽  
Improve Body Composition ◽  
Nutrition And Physical Activity

It is well established that healthy nutrition and physical activity (PA) are key lifestyle factors that modulate lifelong health through their ability to improve body composition, musculoskeletal health, and physical and cognitive performance, as well as to prevent metabolic diseases including obesity, diabetes mellitus, and cardiovascular disease across the lifespan [...]

scholarly journals Could the beneficial effects of dietary calcium on obesity and diabetes control be mediated by changes in intestinal microbiota and integrity?

2015 ◽  
Vol 114 (11) ◽  
pp. 1756-1765 ◽  
Author(s):  
J. M. G. Gomes ◽  
J. A. Costa ◽  
R. C. Alfenas
Keyword(s):  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Beneficial Effects ◽  
Body Weight Reduction ◽  
Intestinal Integrity ◽  
Obesity And Diabetes ◽  
Supplementation Period ◽  
Inflammatory State ◽  
The Impact

AbstractEvidence from animal and human studies has associated gut microbiota, increased translocation of lipopolysaccharide (LPS) and reduced intestinal integrity (II) with the inflammatory state that occurs in obesity and type 2 diabetes mellitus (T2DM). Consumption of Ca may favour body weight reduction and glycaemic control, but its influence on II and gut microbiota is not well understood. Considering the impact of metabolic diseases on public health and the role of Ca on the pathophysiology of these diseases, this review critically discusses possible mechanisms by which high-Ca diets could affect gut microbiota and II. Published studies from 1993 to 2015 about this topic were searched and selected from Medline/PubMed, Scielo and Lilacs databases. High-Ca diets seem to favour the growth of lactobacilli, maintain II (especially in the colon), reduce translocation of LPS and regulate tight-junction gene expression. We conclude that dietary Ca might interfere with gut microbiota and II modulations and it can partly explain the effect of Ca on obesity and T2DM control. However, further research is required to define the supplementation period, the dose and the type of Ca supplement (milk or salt) required for more effective results. As Ca interacts with other components of the diet, these interactions must also be considered in future studies. We believe that more complex mechanisms involving extraintestinal disorders (hormones, cytokines and other biomarkers) also need to be studied.

Metabolic Syndrome and Diabetes Mellitus in Mexico: the Role of PET/CT in Endothelial Dysfunction and Cardiovascular Disease Detection

2017 ◽  
Vol 10 (3) ◽  
Author(s):  
Erick Alexánderson Rosas ◽  
Jonathan Badin Castro ◽  
Diego Adrián Vences Anaya ◽  
Juan José del Moral Díez ◽  
Jessy Steve Masso Bueso ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Disease Detection ◽  
Pet Ct

scholarly journals The Role of Bioactive Peptides in Diabetes and Obesity

Foods ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2220
Author(s):  
Ramachandran Chelliah ◽  
Shuai Wei ◽  
Eric Banan-Mwine Daliri ◽  
Fazle Elahi ◽  
Su-Jung Yeon ◽  
...  
Keyword(s):  
Drug Targets ◽  
Bioactive Peptides ◽  
Metabolic Diseases ◽  
Food Protein ◽  
Protein Fragments ◽  
Obesity And Diabetes ◽  
New Ideas ◽  
Diabetes And Obesity ◽  
Metabolic Syndromes

Bioactive peptides are present in most soy products and eggs and have essential protective functions. Infection is a core feature of innate immunity that affects blood pressure and the glucose level, and ageing can be delayed by killing senescent cells. Food also encrypts bioactive peptides and protein sequences produced through proteolysis or food processing. Unique food protein fragments can improve human health and avoid metabolic diseases, inflammation, hypertension, obesity, and diabetes mellitus. This review focuses on drug targets and fundamental mechanisms of bioactive peptides on metabolic syndromes, namely obesity and type 2 diabetes, to provide new ideas and knowledge on the ability of bioactive peptide to control metabolic syndromes.

scholarly journals The Role of Protein Tyrosine Phosphatase (PTP)-1B in Cardiovascular Disease and Its Interplay with Insulin Resistance

Biomolecules ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. 286 ◽  
Author(s):  
Abdelsalam ◽  
Korashy ◽  
Zeidan ◽  
Agouni
Keyword(s):  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Negative Regulator ◽  
Cardiovascular Disorders ◽  
Protein Tyrosine ◽  
Obesity And Diabetes ◽  
Ptp 1B

Endothelial dysfunction is a key feature of cardiovascular disorders associated with obesity and diabetes. Several studies identified protein tyrosine phosphatase (PTP)-1B, a member of the PTP superfamily, as a major negative regulator for insulin receptor signaling and a novel molecular player in endothelial dysfunction and cardiovascular disease. Unlike other anti-diabetic approaches, genetic deletion or pharmacological inhibition of PTP1B was found to improve glucose homeostasis and insulin signaling without causing lipid buildup in the liver, which represents an advantage over existing therapies. Furthermore, PTP1B was reported to contribute to cardiovascular disturbances, at various molecular levels, which places this enzyme as a unique single therapeutic target for both diabetes and cardiovascular disorders. Synthesizing selective small molecule inhibitors for PTP1B is faced with multiple challenges linked to its similarity of sequence with other PTPs; however, overcoming these challenges would pave the way for novel approaches to treat diabetes and its concurrent cardiovascular complications. In this review article, we summarized the major roles of PTP1B in cardiovascular disease with special emphasis on endothelial dysfunction and its interplay with insulin resistance. Furthermore, we discussed some of the major challenges hindering the synthesis of selective inhibitors for PTP1B.

scholarly journals Endothelial Dysfunction: Is There a Hyperglycemia-Induced Imbalance of NOX and NOS?

2019 ◽  
Vol 20 (15) ◽  
pp. 3775 ◽  
Author(s):  
Cesar A. Meza ◽  
Justin D. La Favor ◽  
Do-Houn Kim ◽  
Robert C. Hickner
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Blood Flow ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Vascular Dysfunction ◽  
Vascular Complications ◽  
Enzymatic Production

NADPH oxidases (NOX) are enzyme complexes that have received much attention as key molecules in the development of vascular dysfunction. NOX have the primary function of generating reactive oxygen species (ROS), and are considered the main source of ROS production in endothelial cells. The endothelium is a thin monolayer that lines the inner surface of blood vessels, acting as a secretory organ to maintain homeostasis of blood flow. The enzymatic production of nitric oxide (NO) by endothelial NO synthase (eNOS) is critical in mediating endothelial function, and oxidative stress can cause dysregulation of eNOS and endothelial dysfunction. Insulin is a stimulus for increases in blood flow and endothelium-dependent vasodilation. However, cardiovascular disease and type 2 diabetes are characterized by poor control of the endothelial cell redox environment, with a shift toward overproduction of ROS by NOX. Studies in models of type 2 diabetes demonstrate that aberrant NOX activation contributes to uncoupling of eNOS and endothelial dysfunction. It is well-established that endothelial dysfunction precedes the onset of cardiovascular disease, therefore NOX are important molecular links between type 2 diabetes and vascular complications. The aim of the current review is to describe the normal, healthy physiological mechanisms involved in endothelial function, and highlight the central role of NOX in mediating endothelial dysfunction when glucose homeostasis is impaired.

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