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Effects of Nutrients on Platelet Function: A Modifiable Link between Metabolic Syndrome and Neurodegeneration?
Arnoldussen, IAC, Witkamp, RF
Biomolecules. 2021;(10)
Abstract
Metabolic syndrome increases the risk of vascular dementia and other neurodegenerative disorders. Recent studies underline that platelets play an important role in linking peripheral with central metabolic and inflammatory mechanisms. In this narrative review, we address the activation of platelets in metabolic syndrome, their effects on neuronal processes and the role of the mediators (e.g., serotonin, platelet-derived growth factor). Emerging evidence shows that nutritional compounds and their metabolites modulate these interactions-specifically, long chain fatty acids, endocannabinoids and phenolic compounds. We reviewed the role of activated platelets in neurovascular processes and nutritional compounds in platelet activation.
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Anthocyanins in berries exhibited anti-atherogenicity and antiplatelet activities in a metabolic syndrome population.
Aboonabi, A, Meyer, RR, Gaiz, A, Singh, I
Nutrition research (New York, N.Y.). 2020;:82-93
Abstract
Metabolic syndrome (MetS) is a global challenge for atherosclerosis. It was hypothesized that a four-week consumption of anthocyanin supplements by MetS patients who had three or more risk factors linked with metabolic syndrome would have a greater improvement in cardiometabolic biomarkers and would also reduce the risk of thrombosis. A total of 55 participants in two groups of Normal healthy and MetS (age 25-75y) were given 320 mg anthocyanin supplements twice daily for 4 weeks. Platelet coagulant activities, lipid profiles, fasting blood glucose, and inflammatory and oxidative stress biomarkers were measured before and after supplementation to evaluate the atheroprotective effects of anthocyanins in the study subjects. Four weeks of anthocyanin supplementation significantly decreased cardiometabolic risk factors including the average serum fasting blood glucose (FBG) (by 13.3%, P < .05) and lipid profiles by significant reduction in triglyceride (by 24.9%, P < .05) and LDL-C (by 33.1%, P < .05) in the MetS group. Anthocyanin supplementation also decreased high sensitivity C-reactive protein (hs-CRP) level (by 28%, P < .05) in females. However, no significant differences in serum UA (uric acid) and HDL-C were observed between anthocyanin pre- and post-treatment in both groups. Moreover, Anthocyanin supplements decreased ADP-induced platelet activation configuration expressed as P-selectin by 40% (P < .05). There was a positive correlation between decreased hs-CRP values and the levels of LDL-C and FBG in the MetS group (P < .05). These results support the hypothesis that anthocyanin supplementation exerts anti-atherogenicity effects by improving cardiometabolic risk factors and reducing thrombogenicity in the MetS population.
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Reduced Lysosomal Acid Lipase Activity in Blood and Platelets Is Associated With Nonalcoholic Fatty Liver Disease.
Ferri, F, Mischitelli, M, Tozzi, G, Messina, E, Mignini, I, Mazzuca, S, Pellone, M, Parisse, S, Marrapodi, R, Visentini, M, et al
Clinical and translational gastroenterology. 2020;(2):e00116
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Abstract
OBJECTIVES To investigate whether blood total lysosomal acid lipase activity (BT-LAL) levels are uniquely associated with the noncirrhotic and cirrhotic stages of nonalcoholic fatty liver disease (NAFLD) and with protection from NAFLD in metabolically/genetically predisposed subjects and a normal liver. To clarify which enzyme-carrying circulating cells are involved in reduced BT-LAL of NAFLD. METHODS In a cross-sectional study, BT-LAL was measured by a fluorigenic method in patients with NAFLD (n = 118), alcoholic (n = 116), and hepatitis C virus-related disease (n = 49), in 103 controls with normal liver and in 58 liver transplant recipients. Intracellular platelet and leukocyte LAL was measured in 14 controls and 28 patients with NAFLD. RESULTS Compared with controls, (i) BT-LAL and LAL in platelets, but not in leukocytes, were progressively reduced in noncirrhotic NAFLD and in nonalcoholic steatohepatitis-related cirrhosis; (ii) platelet and leukocyte counts did not differ in patients with noncirrhotic NAFLD; and (iii) BT-LAL did not differ in alcoholic and hepatitis C virus noncirrhotic patients. BT-LAL progressively increased in controls with metabolic syndrome features according to their PNPLA3 rs738409 steatosis-associated variant status (II vs IM vs MM), and their BT-LAL was higher than that of noncirrhotic NAFLD, only when carriers of the PNPLA3 unfavorable alleles were considered. Liver transplant recipients with de novo NAFLD compared with those without de novo NAFLD had lower BT-LAL. DISCUSSION LAL in blood and platelets is progressively and uniquely reduced in NAFLD according to disease severity. High BT-LAL is associated with protection from NAFLD occurrence in subjects with metabolic and genetic predisposition. Low LAL in platelets and blood could play a pathogenetic role in NAFLD.
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Alterations in platelet function and cell-derived microvesicles in recently menopausal women: relationship to metabolic syndrome and atherogenic risk.
Jayachandran, M, Litwiller, RD, Lahr, BD, Bailey, KR, Owen, WG, Mulvagh, SL, Heit, JA, Hodis, HN, Harman, SM, Miller, VM
Journal of cardiovascular translational research. 2011;(6):811-22
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Abstract
A woman's risk for metabolic syndrome (MS) increases at menopause, with an associated increase in risk for cardiovascular disease. We hypothesized that early menopause-related changes in platelet activity and concentrations of microvesicles derived from activated blood and vascular cells provide a mechanistic link to the early atherothrombotic process. Thus, platelet functions and cellular origin of blood-borne microvesicles in recently menopausal women (n = 118) enrolled in the Kronos Early Estrogen Prevention Study were correlated with components of MS and noninvasive measures of cardiovascular disease [carotid artery intima medial thickness (CIMT), coronary artery calcium (CAC) score, and endothelial reactive hyperemic index (RHI)]. Specific to individual components of the MS pentad, platelet number increased with increasing waist circumference, and platelet secretion of ATP and expression of P-selectin decreased with increasing blood glucose (p = 0.005) and blood pressure (p < 0.05), respectively. Waist circumference and systolic blood pressure were independently associated with monocyte- and endothelium-derived microvesicles (p < 0.05). Platelet-derived and total procoagulant phosphatidylserine-positive microvesicles, and systolic blood pressure correlated with CIMT (p < 0.05), but not with CAC or RHI. In summary, among recently menopausal women, specific platelet functions and concentrations of circulating activated cell membrane-derived procoagulant microvesicles change with individual components of MS. These cellular changes may explain in part how menopause contributes to MS and, eventually, to cardiovascular disease.
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Effects of doxazosin and amlodipine on mean platelet volume and serum serotonin level in patients with metabolic syndrome: a randomised, controlled study.
Demirtunc, R, Duman, D, Basar, M
Clinical drug investigation. 2007;(6):435-41
Abstract
BACKGROUND AND OBJECTIVE In addition to reducing blood pressure, antihypertensive drugs should modify other atherosclerotic risk factors. One such risk factor is the prothrombotic state, which is characterised mainly by increased fibrinogen and plasminogen activator inhibitor-1 levels and abnormalities in platelet function. Platelet activity and aggregation potential can be estimated by measuring mean platelet volume (MPV). Serotonin plays a role in vasospasm and increased platelet aggregation capacity, and has been shown to increase MPV in vitro. However, serotonin levels and MPV have not been studied in the metabolic syndrome. We evaluated mean platelet volume (MPV) in patients with the metabolic syndrome, and compared the effects of doxazosin and amlodipine on MPV and serum serotonin level in patients with this condition. METHODS Thirty-eight patients who met the Adult Treatment Panel III criteria for the metabolic syndrome and 20 healthy controls were included in the study. Patients were randomised into two groups to receive doxazosin 4 mg/day (n=20) or amlodipine 10 mg/day (n=18). Patients' MPV, serum serotonin, insulin, insulin sensitivity, fasting blood glucose and lipid profiles were measured at baseline and after 8 weeks. RESULTS Patients with the metabolic syndrome had a significantly higher MPV compared with the control group. MPV was significantly decreased in the doxazosin-treated group (from 6.9 +/- 1.0 fL at baseline to 6.1 +/- 1.1 fL after treatment; p=0.02) but not in the amlodipine-treated group (6.8 +/- 0.9 fL at baseline vs 6.9 +/- 1.0 fL after treatment; p=0.9). Fasting blood glucose and total cholesterol were also significantly decreased compared with baseline in the doxazosin group. In the amlodipine group, there was a significant increase in serum serotonin levels and a decrease in serum insulin and improved insulin sensitivity. CONCLUSION In patients with the metabolic syndrome, doxazosin treatment not only decreases platelet activity, as measured by a change in MPV, but also improves metabolic abnormalities. Amlodipine also has beneficial effects in patients with the metabolic syndrome but has no effect on MPV.
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Effects of VLDL and remnant particles on platelets.
Olufadi, R, Byrne, CD
Pathophysiology of haemostasis and thrombosis. 2006;(3-4):281-91
Abstract
There is a considerable body of evidence supporting an association between hypertriglyceridaemia, a hypercoagulable state and atherothrombosis. A disorder of triglyceride metabolism is a key feature of the metabolic syndrome that increases risk of both ischaemic heart disease and type 2 diabetes approximately 3-fold. An increasing prevalence of obesity and metabolic syndrome is likely to contribute markedly to the prevalent ischaemic heart in the foreseeable future, and therefore it is crucial to understand mechanisms linking hypertriglyceridaemia and a hypercoagulable state. Activation of platelets and the coagulation cascade are intertwined. VLDL and remnant lipoprotein concentrations are often increased with the metabolic syndrome. These lipoproteins have the capacity to activate platelets and the coagulation pathway, and to support the assembly of the prothrombinase complex. VLDL also upregulates expression of the plasminogen activator inhibitor-1 gene and plasminogen activator inhibitor-1 antigen and activity, a process accompanied by platelet aggregation and clot formation. The surface membrane of activated platelets also supports the assembly and activity of the prothrombinase complex, resulting in further thrombin generation and amplification of the coagulation cascade. Fibrinolysis is also less efficient when thrombin is generated. Thrombin induces thrombin activatable fibrinolysis inhibitor. Thrombin activatable fibrinolysis inhibitor is a carboxypeptidase that cleaves the carboxylic lysine residues on fibrin, thereby abolishing the critical binding site for tPA-plasminogen decreasing plasmin formation. Thus the evidence is supportive of dysregulated coagulation, and impaired fibrinolysis with a predisposition to atherothrombosis, in conditions such as the metabolic syndrome, in which there are increased concentrations of VLDL and remnant lipoproteins. The purpose of this review is to describe the current evidence supporting a procoagulant state induced by VLDL and remnant lipoproteins. The role of these lipoprotein classes in (1) platelet activation; (2) the intrinsic coagulation cascade, and (3) clot formation and fibrinolysis is discussed.
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[The concentration of adenine nucleotides in platelets of patients with primary chronic glomerulonephritis].
Lizakowski, S, Zdrojewski, Z, Jagodziński, P, Słomińska, E, Rutkowski, B
Polskie Archiwum Medycyny Wewnetrznej. 2000;(2):467-73
Abstract
UNLABELLED Nephrotic syndrome (n.s.) is associated with numerous blood coagulation abnormalities and a marked predisposition to thromboembolism. Increased aggregation and activation of platelets in patients with glomerulonephritis (g.l.n. p.t.s.) may partly explain this status. The aim of this study was to measure the platelets adenine nucleotides concentration. The study was performed in 57 patients with a renal biopsy confirmed primary glomerulonephritis and 24 sex and age matched healthy volunteers which served as a control group. The patients were divided into two subgroups: subgroup I/A--36 patients with the symptoms of the nephrotic syndrome and subgroup I/B--21 patients with chronic glomerulonephritis and proteinuria but without the symptoms of nephrotic syndrome. Concentration of adenine nucleotides in platelets was measured using HPLC. In the subgroup I/A significantly lower levels of ATP, ADP and AMP concentrations in platelets were observed comparing to control subjects. Simultaneously significant correlation between both ATP and ADP concentration and plasma levels of albumin, total cholesterol, LDL-cholesterol, triglycerides and fibrinogen were found in g.l.n. p.t.s. SUMMARY AND CONCLUSIONS 1. Significantly lower concentrations of adenine nucleotides in platelets of gln pts with the nephrotic syndrome may result from their activation. 2. Protein and lipid metabolism as well as fibrinogen seem to influence ATP and ADP concentrations in platelets of g.l.n. p.t.s.