Nutritional depletion inn-3 PUFA in apoE knock-out mice: A new model of endothelial dysfunction associated with fatty liver disease

2016 ◽  
Vol 60 (10) ◽  
pp. 2198-2207 ◽  
Author(s):  
Emilie Catry ◽  
Audrey M. Neyrinck ◽  
Irina Lobysheva ◽  
Barbara D. Pachikian ◽  
Matthias Van Hul ◽  
...  
Keyword(s):  
Liver Disease ◽  
Endothelial Dysfunction ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Knock Out ◽  
New Model ◽  
Knock Out Mice ◽  
Nutritional Depletion

scholarly journals LDL Receptor Knock-Out Mice Are a Physiological Model Particularly Vulnerable to Study the Onset of Inflammation in Non-Alcoholic Fatty Liver Disease

PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e30668 ◽  
Author(s):  
Veerle Bieghs ◽  
Patrick J. Van Gorp ◽  
Kristiaan Wouters ◽  
Tim Hendrikx ◽  
Marion J. Gijbels ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Ldl Receptor ◽  
Physiological Model ◽  
Alcoholic Fatty Liver ◽  
Knock Out ◽  
Knock Out Mice ◽  
Alcoholic Fatty Liver Disease

scholarly journals Non-alcoholic fatty liver disease may be associated with endothelial dysfunction

2013 ◽  
Vol 119 (1) ◽  
pp. 57-57 ◽  
Author(s):  
Sevket Balta ◽  
Sait Demirkol ◽  
Zekeriya Arslan ◽  
Mustafa Demir ◽  
Murat Unlu ◽  
...  
Keyword(s):  
Liver Disease ◽  
Endothelial Dysfunction ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

scholarly journals PECULIARITIES OF SYSTEMIС INFLAMMATION OF LOW INTENSITY IN PATIENTS WITH STABLE CORONARY HEART DISEASE CONCURRENT WITH NON-ALCOHOLIC FATTY LIVER DISEASE

2019 ◽  
Vol 23 (3-4) ◽  
pp. 3-6 ◽  
Author(s):  
Yu.I. Manusha ◽  
Yu.M. Kazakov ◽  
Т.А. Trybrat ◽  
K.E. Ischeykin
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Liver Disease ◽  
Endothelial Dysfunction ◽  
Fatty Liver ◽  
Systemic Inflammation ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Low Intensity ◽  
Alcoholic Fatty Liver Disease

Nowadays, coronary heart disease and non-alchoholic fatty liver disease are significant problems in Ukraine and world. Functional liver disorders potentiate the development and progression of CHD. The initiation process of atherosclerosis is a chronic systemic inflammation of low intensity. This view on atherosclerosis development has been forming during the past two decades. The aim of the research was to study the features/characteristics of systemic inflammation of low intensity in patients with coronary heart disease in combination with non-alcoholic fatty liver disease. The research involved 135 people with CHD: stable angina, I-II functional class, 0-I heart failure in combination with non-alcoholic fatty liver disease and 30 healthy individuals. We examined patients in terms of blood levels of cytokines -TNFα and IL-10, the content of the acute phase reactant and the coagulation factor, the marker of endothelial dysfunction is the amount of circulating endothelial microparticles (CEM) CD32+ CD40+ and the expression level of IkBα gene NF-kB in mononuclear peripheral blood. We studied the level of expression of the mRNA gene of IkBα in mononuclear cells, which reflects the level of transcriptional activity of NF-kB in patients with stable coronary artery disease and CHD in combination with NAFLD showed a significant increase in the expression of the mRNA gene of IkBα by 88.5% compared to patients with stable stable coronary heart disease. The analysis of the functional state of the endothelium with help of CEM CD32+ CD40+ has shown the presence of endothelial dysfunction in the groups of patients with CHD and CHD in combination with of NAFLD. Comparison of the indicators of systemic inflammation of low intensity and marker of endothelial dysfunction in patients with CHD in combination with NAFLD revealed a significant increase of TNFα, acute phase reactant and coagulation fibrinogen factor and expression of the mRNA IkBα gene in patients with comorbidity, indicating an increase the level of systemic inflammation of low intensity in patients with CHD in combination with NAFLD as compared with the group of patients with CHD.

scholarly journals Endothelial dysfunction in nonalcoholic fatty liver disease

2021 ◽  
Vol 3 (1) ◽  
pp. 4-10
Author(s):  
Angela PELTEC ◽  
Murad ALNABGHALIE
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Liver Disease ◽  
Endothelial Dysfunction ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Ldl Receptor ◽  
Pentraxin 3 ◽  
Nonalcoholic Fatty Liver

Introduction. The prevalence of nonalcoholic fatty liver disease (NAFLD) in western countries is increasing rapidly and is considered as component of metabolic syndrome. Endothelial dysfunction is a pathophysiological problem of cardiovascular disease. NAFLD, as a component of metabolic syndrome, is associated with endothelial dysfunction. Material and methods. PubMed database was used in order to review and select articles according to the keywords. A total of 216 articles matching search criteria were found between 2000-2021. Results. The present study has been underlined the role of pathophysiological mechanisms of endothelial dysfunction in nonalcoholic fatty liver disease, which involves oxidative stress, inflammation and insulin resistance. The main factor in the occurrence of endothelial dysfunction is related to nitric oxide (NO) biosynthesis. The markers associated with regulation of nitric oxide biosynthesis, such as asymmetric dimethylarginine, free fatty acid, lectin-like oxidized low-density lipoprotein (LDL) receptor-1 and pentraxin-3, are potential targets in the assessment of endothelial dysfunction. Conclusions. Insulin resistance, inflammation and oxidative stress have been involved in the reduction of NO biosynthesis that influences the occurrence of endothelial dysfunction. Markers, such as lectin-like oxidized LDL receptor-1 and pentraxin-3, have been considered as potential targets in the assessment of endothelial dysfunctions in NAFLD.

Sign in / Sign up

Export Citation Format

Share Document