scholarly journals Effect of a plant sterol-enriched spread on biomarkers of endothelial dysfunction and low-grade inflammation in hypercholesterolaemic subjects

2016 ◽  
Vol 5 ◽  
Author(s):  
R. T. Ras ◽  
D. Fuchs ◽  
W. P. Koppenol ◽  
C. G. Schalkwijk ◽  
A. Otten-Hofman ◽  
...  

AbstractPlant sterols (PS) lower LDL-cholesterol, an established risk factor for CHD. Endothelial dysfunction and low-grade inflammation are two important features in the development of atherosclerosis. Whether PS affect biomarkers of endothelial function and low-grade inflammation is not well studied. The aim of the present study was to investigate the effect of regular intake of PS on biomarkers of endothelial dysfunction and low-grade inflammation. In a double-blind, randomised, placebo-controlled, parallel-group study, which was primarily designed to investigate the effect of PS intake on vascular function (clinicaltrials.gov: NCT01803178), 240 hypercholesterolaemic but otherwise healthy men and women consumed a low-fat spread with added PS (3 g/d) or a placebo spread for 12 weeks. Endothelial dysfunction biomarkers (both vascular and intracellular adhesion molecules 1 and soluble endothelial-selectin) and low-grade inflammation biomarkers (C-reactive protein, serum amyloid A, IL-6, IL-8, TNF-α and soluble intercellular adhesion molecule-1) were measured using a multi-array detection system based on electrochemiluminescence technology. Biomarkers were combined using z-scores. Differences in changes from baseline between the PS and the placebo groups were assessed. The intake of PS did not significantly change the individual biomarkers of endothelial dysfunction and low-grade inflammation. The z-scores for endothelial dysfunction (−0·02; 95 % CI −0·15, 0·11) and low-grade inflammation (−0·04; 95 % CI −0·16, 0·07) were also not significantly changed after PS intake compared with placebo. In conclusion, biomarkers of endothelial dysfunction and low-grade inflammation were not affected by regular intake of 3 g/d PS for 12 weeks in hypercholesterolaemic men and women.

2015 ◽  
Vol 114 (11) ◽  
pp. 1819-1828 ◽  
Author(s):  
Karianna F. M. Teunissen-Beekman ◽  
Janneke Dopheide ◽  
Johanna M. Geleijnse ◽  
Stephan J. L. Bakker ◽  
Elizabeth J. Brink ◽  
...  

AbstractEndothelial dysfunction (ED) and low-grade inflammation (LGI) have a role in the development of CVD. The two studies reported here explored the effects of dietary proteins and carbohydrates on markers of ED and LGI in overweight/obese individuals with untreated elevated blood pressure. In the first study, fifty-two participants consumed a protein mix or maltodextrin (3×20 g/d) for 4 weeks. Fasting levels and 12 h postprandial responses of markers of ED (soluble intercellular adhesion molecule 1 (sICAM), soluble vascular cell adhesion molecule 1 (sVCAM), soluble endothelial selectin and von Willebrand factor) and markers of LGI (serum amyloid A, C-reactive protein and sICAM) were evaluated before and after intervention. Biomarkers were also combined into mean Z-scores of ED and LGI. The second study compared 4 h postprandial responses of ED and LGI markers in forty-eight participants after ingestion of 0·6 g/kg pea protein, milk protein and egg-white protein. In addition, postprandial responses after maltodextrin intake were compared with a protein mix and sucrose. The first study showed significantly lower fasting ED Z-scores and sICAM after 4 weeks on the high-protein diet (P≤0·02). The postprandial studies found no clear differences of ED and LGI between test meals. However, postprandial sVCAM decreased more after the protein mix compared with maltodextrin in both studies (P≤0·04). In conclusion, dietary protein is beneficial for fasting ED, but not for fasting LGI, after 4 weeks of supplementation. On the basis of Z-scores, postprandial ED and LGI were not differentially affected by protein sources or carbohydrates.


2005 ◽  
Vol 64 (1) ◽  
pp. 15-22 ◽  
Author(s):  
Atul Singhal

Atherosclerotic CVD is the most common cause of death in the West. Yet, its pathogenesis and early development are only partially understood. Central to the early atherosclerotic process is impairment of vascular endothelial function. Endothelial dysfunction can be measured non-invasively and is evident in children before clinical manifestations of atherosclerosis in adulthood. Factors in early life, such as conventional cardiovascular risk factors, or programming by perinatal growth and nutrition strongly affect endothelial function and hence the development of atherosclerosis and CVD. For instance, low birth weight and faster growth early in infancy have a detrimental effect on vascular structure and function. Childhood obesity, a key independent risk factor for CVD, also adversely affects early vascular health. Obesity is associated with endothelial dysfunction and greater arterial stiffness from as early as the first decade of life, while weight loss is beneficial. This effect on vascular function is probably mediated in part by low-grade inflammation and insulin resistance associated with obesity or by the production by adipose tissue of cytokine-like molecules, collectively termed adipokines. A high leptin concentration, in particular, is found in obese individuals and is strongly associated with vascular changes related to early atherosclerosis. The present review focuses on the early origins of endothelial dysfunction, emphasising the role of obesity. It also considers the mechanisms by which obesity impairs endothelial function, understanding of which will be important to further scientific knowledge and to improve public health.


2020 ◽  
Vol 26 (32) ◽  
pp. 3955-3972
Author(s):  
Ecem Kaya-Sezginer ◽  
Serap Gur

Background: Erectile dysfunction (ED) is an evolving health problem in the aging male population. Chronic low-grade inflammation is a critical component of ED pathogenesis and a probable intermediate stage of endothelial dysfunction, especially in metabolic diseases, with the inclusion of obesity, metabolic syndrome, and diabetes. Objective: This review will present an overview of preclinical and clinical data regarding common inflammatory mechanisms involved in the pathogenesis of ED associated with metabolic diseases and the effect of antiinflammatory drugs on ED. Methods: A literature search of existing pre-clinical and clinical studies was performed on databases [Pubmed (MEDLINE), Scopus, and Embase] from January 2000 to October 2019. Results: Low-grade inflammation is a possible pathological role in endothelial dysfunction as a consequence of ED and other related metabolic diseases. Increased inflammation and endothelial/prothrombotic markers can be associated with the presence and degree of ED. Pharmacological therapy and modification of lifestyle and risk factors may have a significant role in the recovery of erectile response through reduction of inflammatory marker levels. Conclusion: Inflammation is the least common denominator in the pathology of ED and metabolic disorders. The inflammatory process of ED includes a shift in the complex interactions of cytokines, chemokines, and adhesion molecules. These data have established that anti-inflammatory agents could be used as a therapeutic opportunity in the prevention and treatment of ED. Further research on inflammation-related mechanisms underlying ED and the effect of therapeutic strategies aimed at reducing inflammation is required for a better understanding of the pathogenesis and successful management of ED.


Hypertension ◽  
2011 ◽  
Vol 58 (4) ◽  
pp. 588-595 ◽  
Author(s):  
Bas C. van Bussel ◽  
Fleur Schouten ◽  
Ronald M. Henry ◽  
Casper G. Schalkwijk ◽  
Michiel R. de Boer ◽  
...  

2007 ◽  
Vol 24 (9) ◽  
pp. 969-976 ◽  
Author(s):  
A. M. W. Spijkerman ◽  
M.-A. Gall ◽  
L. Tarnow ◽  
J. W. R. Twisk ◽  
E. Lauritzen ◽  
...  

2019 ◽  
Author(s):  
Haoyue Shi ◽  
Deshuang Yang ◽  
Jiajun Qiao ◽  
Rui Sun ◽  
Ruihan Li ◽  
...  

Abstract Background Hypertension is an important worldwide public health challenge because of its high prevalence and concomitant risks of cardiovascular disease. It induces half of the coronary heart disease and approximately two-thirds of the cerebrovascular disease burdens. Vascular endothelial dysfunction plays important roles in the pathophysiology of essential hypertension. Sang-qi Granules (SQG), a Chinese herbal formula, is used to treat I or II hypertension. Several animal experimental studies have shown that SQG can lower blood pressure and myocardial fibrosis by suppressing inflammatory responses. However, there is no standard clinical trial to confirm this and whether SQG can improve endothelial cell function is unknown.Methods In this randomized, double-blind, double-simulation controlled trial, 300 patients with stage I or II hypertension will be recruited and randomly allocated in a 1:1:1 ratio to group A(treatment with SQG and placebo of Cozaar), group B (treatment with Cozaar and placebo of SQG), and group C (treatment with SQG and Cozaar). SQG (or its placebo) will be administrated twice a day at the doze of 10g each time, and 50mg Cozaar(or its placebo) will be administrated once in the morning. The primary endpoint is the drug efficiency of the each three groups. The secondary endpoints are the change of average systolic and diastolic blood pressure during the day and the night, the change of blood pressure drop rate at night, target organ damage assessment (heart rate variability, ankle-brachial index and pulse wave velocity), symptoms improvement assessment (hypertension symptom scale, TCM syndrome integral scale, Pittsburgh sleep quality index scale, Self-Rating Anxiety Scale, Self-Rating Depression Scale and the Short Form-36 Health Survey), blood lipids, serum indicators of vascular function (changes in serum ET-1, TXA2, NO, PGI2 values) and safety indicators.Discussion This study will provide clinical evidence for the efficacy and safety of SQG in the treatment of hypertension. Meanwhile, the possible mechanism of SQG for lowering blood pressure will be further explored by observing the protective effect of SQG on vascular endothelial function, as well as its effect on related clinical symptoms, risk factors and target organs of hypertension.


Author(s):  
Steven A. Bloomer ◽  
Eric Moyer

Aging is associated with chronic, low-grade inflammation that adversely affects physiological function. The liver regulates systemic inflammation; it is a source of cytokine production and also scavenges bacteria from the portal circulation to prevent infection of other organs. The cells with primary roles in these functions, hepatic macrophages, become more numerous in the liver with "normal" aging (i.e. in the absence of disease). Here we demonstrate evidence and potential mechanisms for this phenomenon, which include augmented tumor necrosis factor-α (TNFα) and intercellular adhesion molecule-1 (ICAM-1) expression in the liver. Also, we discuss how an age-related impairment in autophagy within macrophages leads to a pro-oxidative state and ensuing production of pro-inflammatory cytokines, particularly interleukin 6 (IL-6). Given that the liver is a rich source of macrophages, we posit that it represents a major source of the elevated systemic IL-6 observed with aging, which is associated with physiological dysfunction. Testing a causal role for liver macrophage production of IL-6 during aging remains a challenge, yet interventions that have targeted macrophages and/or IL-6 have demonstrated promise in treating age-related diseases. These studies have demonstrated an age-related, deleterious reprogramming of macrophage function, which worsens pathology. Therefore, hepatic macrophage accrual is indeed a cause for concern, and therapies that attenuate the aged phenotype of macrophages will likely prove useful in promoting healthy aging.


2013 ◽  
Vol 44 (7) ◽  
pp. 1403-1416 ◽  
Author(s):  
T. T. van Sloten ◽  
M. T. Schram ◽  
M. C. Adriaanse ◽  
J. M. Dekker ◽  
G. Nijpels ◽  
...  

BackgroundEndothelial dysfunction (ED), low-grade inflammation (LGI) and oxidative stress (OxS) may be involved in the pathobiology of depression. Previous studies on the association of these processes in depression have yielded contradictory results. We therefore investigated comprehensively, in a population-based cohort study, the association between ED, LGI and OxS on the one hand and depressive symptoms on the other.MethodWe used data from the Hoorn Study and determined biomarkers of ED [flow-mediated dilatation (FMD), von Willebrand factor, soluble intercellular adhesion molecule 1 (sICAM-1), soluble vascular cell adhesion molecule 1, soluble thrombomodulin and soluble endothelial selectin], LGI [C-reactive protein, tumour necrosis factor-α, interleukin 6, interleukin 8, serum amyloid A, myeloperoxidase (MPO) and sICAM-1] and OxS (oxidized low density lipoprotein and MPO). Depressive symptoms were quantified by the Center for Epidemiologic Studies Depression Scale (CES-D) questionnaire (n = 493; age 68 years; 49.9% female). Regression analyses were performed with the use of biomarker Z scores. Adjustments were made for age, sex and glucose metabolism status (cohort stratification variables) and prior cardiovascular disease, hypertension, waist-to-hip ratio, cholesterol levels, education level, physical activity, dietary habits, and the use of antihypertensive and/or lipid-lowering medication and/or metformin (potential confounders).ResultsAfter adjustment for age, sex and glucose metabolism status, one standard deviation increase in the ED Z score was associated with a 1.9 [95% confidence interval (CI) 0.7–3.1] higher CES-D score. Additional adjustments did not materially change this result. LGI and OxS were not associated with the CES-D score.ConclusionsED, as quantified by an array of circulating biomarkers and FMD, was independently associated with depressive symptoms. This study supports the hypothesis that ED plays an important role in the pathobiology of depression.


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