Blood coagulation and aortic wall integrity in rats with obesity-induced insulin resistance

Dziuba, O. S.

doi:10.15407/ubj90.02.014

Cited by 5 publications

(4 citation statements)

References 40 publications

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“…At the end of the intervention, examination showed that the thickness of aorta rose in high-fat diet and that this increase was followed by endothelial damage in the form of alteration of endothelial lining and edema formation. 28 Other studies also showed that high-fructose or high-fat diet given for 8 weeks resulted in the thickening of abdominal aortic in 32 Sprague Dawley rats and increased aorta lesion by 40% higher than the control group of 29 WHHL/Watanabe Heritable Hyperlipidemic rabbits. 11 , 29 HFFD can also lead to the alteration of lipid serum, which is significantly associated with aorta thickening.…”

Section: Resultsmentioning

confidence: 94%

High-Fructose Diet Initially Promotes Increased Aortic Wall Thickness, Liver Steatosis, and Cardiac Histopathology Deterioration, but Does Not Increase Body Fat Index

Handayani

Febrianingsih

Kurniawati

et al. 2021

Journal of Public Health Research

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Background: Dietary fats and fructose have been responsible for inducing obesity and body tissues damage due to the consequence of metabolic syndrome through several mechanisms. The body fat index (BFI) is one of the anthropometric measures used to detect obesity in rats. This study aims to examine the correlation between high-fat high-fructose diet and liver steatosis cell count, early atherosclerosis characteristics, and BFI in Sprague Dawley Rats.Design and methods: This was an experimental design using 2 groups of 12-weeks-old Sprague Dawley (SD) rats. The control group received a standard diet and tap water beverages for 17 weeks. The intervention group was fed with high-fat diet from modified AIN 93-M and additional 30% fructose drink. We analyzed the foam cell count, aortic wall thickness, cardiac histopathology, and liver steatosis cell count after the sacrifice process.Results: The rats in the intervention group had a higher aortic wall thickness, liver steatosis, and foam cell count (+125%, p<0.01; +317%, p<0.01 and +165%, p<0.01 respectively) compared to the control group. The intervention group also showed higher mononuclear inflammatory and hypertrophic cell count. A significant positive correlation was found between dietary fructose with premature atherosclerosis by increasing foam cell count (r=0.66) and aortic wall thickness (r=0.68). In addition, 30% dietary fructose increased liver steatosis (r =0.69) and mononuclear inflammatory cardiac cell count (r=0.61). Interestingly, the intervention had no effect on BFI (p>0.5; r=0.13).Conclusions: Dietary fat and fructose consumption for 17 weeks promote atherosclerosis, liver steatosis, and cardiac histopathology alteration without increasing BFI.

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Section: Resultsmentioning

confidence: 94%

High-Fructose Diet Initially Promotes Increased Aortic Wall Thickness, Liver Steatosis, and Cardiac Histopathology Deterioration, but Does Not Increase Body Fat Index

Handayani

Febrianingsih

Kurniawati

et al. 2021

Journal of Public Health Research

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“…Instead of inhibiting blood coagulation, we used an anti-inflammatory agent. No one could predict that the endogenously produced fatty acid compound NSE can inhibit blood coagulation, omitting its moderate anti-aggregatory effect on platelets [30]. However its anti-inflammatory effects are well known and widely studied.…”

Section: Discussionmentioning

confidence: 99%

Protective action of N-stearoylethanolamine on blood coagulation and arterial changes in spontaneously hypertensive rats fed cholesterol-rich diet

Tkachenko¹,

Hudz²,

Kosiakova³

et al. 2020

Ukr.Biochem.J.

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In this work we aimed to test the atherosclerotic changes in the aortic wall and pro-coagulant response of the blood coagulation system of spontaneously hypertensive rats (Shr) fed cholesterol-rich diet (CRD) and to study the effect of the anti-inflammatory agent N-stearoylethanolamine (NSE) on the development of atherosclerosis in this model. Female rats (n = 30) with genetically determined hypertension proven by direct measurement of blood pressure were fed crd (5% cholesterol) for 2 months. control group of Shr (n = 10) received standard pellet diet, 10 were fed crd and 10 received crd with daily per os application of NSe at a dose of 50 mg/kg of body weight. histological analysis detected swelling and detachment of endothelial cells, huge edema of the subendothelial layer and a disruption of the middle shell integrity. crd rats had higher fibrinogen concentration, increased rate of platelet aggregation and decreased level of anticoagulant Pc. Platelet aggregation speed increased in crd-fed rats (52.5±4.1%/min) was slightly normalized under the action of NSe (40±8.3 vs 35±9%/min in controls). Fibrinogen concentration was slightly increased in crdfed rats (2.75±0.7 vs 1.9±0.5 mg/ml in controls). however, the level of anticoagulant Pc that was decreased in crd-fed rats (65±16 vs 100±11% in controls) was normalized under the action of NSe (92±17%). NSe also influenced the aorta architecture, however normalizing the thickness of the aorticwall did not change the cholesterol-induced inclusions within aorta media. NSE anti-inflammatory action changes the atherogenic processes in CRD-fed rats mainly protecting PC from consumption during the inflammatory process and reducing edema of the aorta. however hematological parameters (including clotting time in the aPTT test and fibrinogen concentration) changed independently on NSE application. Anti-aggregatory action of NSE on platelets can be a result of direct action on platelets or the consequence of its anti-inflammatory action. During atherogenesis induced by CRD in the model, NSE demonstrated valuable anti-inflammatory action protecting the organism during atherogenesis, however it cannot be assumed as an antithrombotic or antiatherogenic agent because it is unable to influence hemostasis directly. k e y w o r d s: atherosclerosis, cholesterol-rich diet, N-stearoylethanolamine (NSe), hemostasis.

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“…Previously we developed and characterized a model of obesity-induced insulin resistance in rats. Alongside with changes in blood coagulation parameters, this condition was shown to cause the over-reactivity of platelets (Dziuba et al, 2018). In the current study, we measured the aggregation of platelets from obese IR rats and compared it to that from rats that had been given NSE per os for two weeks until the end of the experiment.…”

Section: Nse Administration Leads To Normalization Of Platelet Aggreg...mentioning

confidence: 96%

N-Stearoylethanolamine Inhibits Integrin-Mediated Activation, Aggregation, and Adhesion of Human Platelets

Hudz

Chernyshenko

Kasatkina

et al. 2022

J Pharmacol Exp Ther

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N-stearoylethanolamine (NSE), a lipid mediator that belongs to the N-acylethanolamine (NAE) family, has anti-inflammatory, antioxidant and membranoprotective actions. In contrast to other NAEs, NSE does not interact with cannabinoid receptors. The exact mechanism of its action remains unclear. The aim of this study was to evaluate the action of NSE on activation, aggregation and adhesion of platelets that were chosen as a model of cellular response.Aggregation of platelets was measured to analyze the action of NSE (10 -6 -10 -10 M) on platelet reactivity. Changes in granularity and shape of resting platelets and platelets stimulated with ADP in the presence of NSE were monitored by flow-cytometry, platelet deganulation was monitored by spectrofluorimetry. In vivo studies were performed using obese insulin-resistant rats. Binding of fibrinogen to the GPIIb/IIIa receptor was estimated using indirect ELISA and scanning electron microscopy (SEM). It was found that NSE inhibits the activation and aggregation of human platelets. Our results suggest that NSE may decrease the activation and subsequent aggregation of platelets induced by ristocetin, epinephrine and low doses of ADP.NSE also reduced the binding of fibrinogen to GPIIb/IIIa on activated platelets. These effects could be explained by the inhibition of platelet activation mediated by integrin receptors: the GPIb-IX-V complex for ristocetin-induced activation and GPIIb/IIIa when epinephrine and low doses of ADP were applied. The anti-platelet effect of NSE complements its anti-inflammatory effect and allows us to prioritize studies of NSE as a potent anti-thrombotic agent. Significance StatementN-stearoylethanolamine (NSE) was shown to possess inhibitory action on platelet activation, adhesion and aggregation. The mechanism of inhibition possibly involves integrin receptors. This finding complements the known anti-inflammatory effects of NSE.

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Blood coagulation and aortic wall integrity in rats with obesity-induced insulin resistance

Cited by 5 publications

References 40 publications

High-Fructose Diet Initially Promotes Increased Aortic Wall Thickness, Liver Steatosis, and Cardiac Histopathology Deterioration, but Does Not Increase Body Fat Index

High-Fructose Diet Initially Promotes Increased Aortic Wall Thickness, Liver Steatosis, and Cardiac Histopathology Deterioration, but Does Not Increase Body Fat Index

Protective action of N-stearoylethanolamine on blood coagulation and arterial changes in spontaneously hypertensive rats fed cholesterol-rich diet

N-Stearoylethanolamine Inhibits Integrin-Mediated Activation, Aggregation, and Adhesion of Human Platelets

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