scholarly journals Overproduction of Very Low–Density Lipoproteins Is the Hallmark of the Dyslipidemia in the Metabolic Syndrome

2008 ◽  
Vol 28 (7) ◽  
pp. 1225-1236 ◽  
Author(s):  
Martin Adiels ◽  
Sven-Olof Olofsson ◽  
Marja-Riitta Taskinen ◽  
Jan Borén
Keyword(s):  
Metabolic Syndrome ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
The Metabolic Syndrome

scholarly journals Reactivity features of cytokines and vasculoendothelial growth factor in patients with chronic cerebral ischemia and metabolic syndrome

2019 ◽  
Keyword(s):  
Metabolic Syndrome ◽  
Cerebral Ischemia ◽  
Growth Factor ◽  
Waist Circumference ◽  
Interleukin 6 ◽  
Interleukin 10 ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Chronic Cerebral Ischemia ◽  
Very Low Density Lipoproteins

The purpose of the research is to determine the correlation between cytokines (interleukin-6, interleukin-10), vasculoendothelial growth factor, biochemical and anthropometric parameters in patients with chronic cerebral ischemia and metabolic syndrome. We examined 77 patients with chronic cerebral ischemia divided into 2 groups: with metabolic syndrome and without metabolic syndrome. In addition to neuroimaging, anthropometric and biochemical research we determined serum concentrations of interleukin-6, interleukin-10 and vasculoendothelial growth factor. It was found that patients with chronic cerebral ischemia and metabolic syndrome had significantly higher concentrations of interleukin-6, vasculoendothelial growth factor, indicators of weight, body mass index, waist circumference, glucose concentration, triglycerides, very low density lipoproteins, and high density lipoproteins was lower compared with the group without metabolic syndrome. During the comparing process of the biomarkers concentrations depending on gender, it was found that in patients with chronic cerebral ischemia and metabolic syndrome, the concentration of interleukin-6 was significantly higher in women than in men. Examination of all patients with chronic cerebral ischemia showed a direct correlation between the concentrations of interleukin-6 and glucose, the concentrations of interleukin-6 and weight, the concentrations of interleukin-6 and the waist circumference and between the concentration of vasculoendothelial growth factor and the waist circumference, in the group with metabolic syndrome - between the concentrations of interleukin-6 and interleukin-10, and in the group without metabolic syndrome - between the waist circumference and the atherogenic coefficient, between the concentrations of low density lipoproteins and β-lipoproteids, between the concentrations of low density lipoproteins and very low density lipoproteins. Thereby, metabolic syndrome is an additional complicating factor that comprehensively affects the reactivity of cytokines and vasculoendothelial growth factor in the pathogenesis of chronic cerebral ischemia.

scholarly journals Role of vascular endothelial growth factor in the pathogenesis of hepatic steatosis and dyslipidemia

2020 ◽  
pp. 31-36
Author(s):  
И.Л. Гуляева ◽  
И.А. Булатова ◽  
Л.Д. Пестренин
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Low Density Lipoproteins ◽  
Control Group ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Fatty Liver Index ◽  
Nonalcoholic Hepatic Steatosis ◽  
Hepatic Steatosis Index

Цель исследования - изучение роли васкулоэндотелиального фактора роста в патогенезе неалкогольного стеатоза печени и дислипидемии при метаболическом синдроме. Методика. Обследовано 35 пациентов с неалкогольным стеатозом печени, в том числе 22 женщины и 13 мужчин. Группу контроля составили 12 сопоставимых по полу и возрасту лиц без патологии печени и признаков метаболического синдрома. Наличие жирового гепатоза подтверждали методом ультразвукового исследования. У пациентов с патологией печени рассчитывали индексы-предикторы стеатоза: Fatty Liver Index (FLI) и Hepatic Steatosis Index (HSI). У всех участников исследования определяли уровни провоспалительных цитокинов и васкулоэндотелиального фактора роста (ВЭФР), оценивали также липидный спектр крови и функциональные печеночные пробы. Результаты. У пациентов со стеатозом печени наблюдалось значимое увеличение уровней провоспалительных цитокинов, ВЭФР, общего холестерина и липопротеинов низкой и очень низкой плотности. Индекс атерогенности также был значимо выше, чем в контрольной группе. Концентрация ВЭФР положительно коррелировала с показателями окружности талии, тимоловой пробы, уровнями общего холестерина, липопротеинов низкой плотности и индексом атерогенности. Чувствительность FLI составила 91,4%, HSI - 97,1%. При этом, значения FLI и HSI значимо коррелировали с уровнем ВЭФР. Заключение. Полученные данные позволяют предположить, что ВЭФР, один из основных маркеров эндотелиальной дисфункции, может играть немаловажную роль в патогенезе неалкогольного стеатоза печени и дислипидемии у пациентов с метаболическомим синдромом The aim of the study was to assess the role of vascular endothelial growth factor (VEGF) in the pathogenesis of nonalcoholic hepatic steatosis and dyslipidemia in patients with signs of metabolic syndrome. Methods. 35 patients with nonalcoholic fatty liver disease, including 22 women and 13 men, were evaluated. The sex- and age-matched control group consisted of 12 people without liver pathology and metabolic syndrome criteria. Presence of hepatic steatosis was confirmed by an ultrasound examination. The Fatty Liver Index (FLI) and the Hepatic Steatosis Index (HSI) were calculated for patients with hepatic steatosis. Concentrations of proinflammatory cytokines and VEGF were measured for all participants. Also, blood biochemistry, including the lipid profile and liver function tests, was analyzed. Results. In patients with hepatic steatosis, levels of proinflammatory cytokines and VEGF were significantly increased. Also, concentrations of total cholesterol, low-density lipoproteins, and very low-density lipoproteins were higher in patients with the liver pathology than in the control group. Atherogenic coefficient was increased in hepatic steatosis. Significant correlations were observed between VEGF and waist circumference, thymol test, total cholesterol, low-density lipoproteins, very low-density lipoproteins, and atherogenic coefficient. Sensitivity of FLI and HIS was 91.4% and 97.1%, respectively. Also, FLI significantly correlated with HSI and VEGF level. Conclusion. The study suggested that VEGF, of the main markers of endothelial dysfunction, plays an important role in the pathogenesis of nonalcoholic hepatic steatosis and dyslipidemia in patients with signs of metabolic syndrome.

Triglyceride Management in Cardiovascular Risk Reduction

2005 ◽  
Vol 00 (01) ◽  
pp. 31
Author(s):  
Michael Miller
Keyword(s):  
Metabolic Syndrome ◽  
Risk Factor ◽  
Cardiovascular Risk ◽  
Ldl Cholesterol ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
The Metabolic Syndrome ◽  
Ldl Particles

Elevated triglycerides are now considered an independent risk factor for coronary heart disease (CHD), even apart from elevated low-density lipoprotein (LDL) cholesterol. While the primary lipid target for CHD risk management remains LDL cholesterol, the treatment of elevated triglycerides is now also recommended. Elevated triglycerides are believed to increase cardiovascular risk because certain triglyceride-rich lipoproteins, called remnant lipoproteins (partially degraded chylomicrons and very-low density lipoproteins (VLDL)), are atherogenic. Hypertri-glyceridemia, together with low levels of high-density lipoprotein (HDL) cholesterol and an increased prevalence of small, dense LDL particles, comprise a triad of lipid risk factors known as atherogenic dyslipidemia.The significance of hypertriglyceridemia as a cardiovascular risk factor is further highlighted by its inclusion as a component of the metabolic syndrome, a cluster of metabolic abnormalities, related to insulin resistance. The other criteria for metabolic syndrome include low HDL cholesterol, central obesity, elevated blood pressure, and abnormal fasting glucose. The metabolic syndrome is recognized as a major risk factor not only for premature CHD but also for type 2 diabetes mellitus.

scholarly journals Very Low-Density Lipoproteins of Metabolic Syndrome Modulates STIM1, Suppresses Store-Operated Calcium Entry, and Deranges Myofilament Proteins in Atrial Myocytes

2019 ◽  
Vol 8 (6) ◽  
pp. 881 ◽  
Author(s):  
Yi-Lin Shiou ◽  
Hsin-Ting Lin ◽  
Liang-Yin Ke ◽  
Bin-Nan Wu ◽  
Shyi-Jang Shin ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Metabolic Syndrome ◽  
Calcium Release ◽  
Nuclear Translocation ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Atrial Myocytes ◽  
Very Low Density Lipoproteins ◽  
Activated T Cells

Individuals with metabolic syndrome (MetS) are at high risk for atrial myopathy and atrial fibrillation. Very low-density lipoproteins (VLDLs) of MetS (MetS-VLDLs) are cytotoxic to atrial myocytes in vivo and in vitro. The calcineurin–nuclear factor of activated T-cells (NFAT) pathway, which is regulated by stromal interaction molecule 1 (STIM1)/ calcium release-activated calcium channel protein 1 (Orai1)–mediated store-operated Ca2+ entry (SOCE), is a pivotal mediator of adaptive cardiac hypertrophy. We hypothesized that MetS-VLDLs could affect SOCE and the calcineurin–NFAT pathway. Normal-VLDL and MetS-VLDL samples were isolated from the peripheral blood of healthy volunteers and individuals with MetS. VLDLs were applied to HL-1 atrial myocytes for 18 h and were also injected into wild-type C57BL/6 male mouse tails three times per week for six weeks. After the sarcoplasmic reticulum (SR) Ca2+ store was depleted, SOCE was triggered upon reperfusion with 1.8 mM of Ca2+. SOCE was attenuated by MetS-VLDLs, along with reduced transcriptional and membranous expression of STIM1 (P = 0.025), and enhanced modification of O-GlcNAcylation on STIM1 protein, while Orai1 was unaltered. The nuclear translocation and activity of calcineurin were both reduced (P < 0.05), along with the alteration of myofilament proteins in atrial tissues. These changes were absent in normal-VLDL-treated cells. Our results demonstrated that MetS-VLDLs suppressed SOCE by modulating STIM1 at the transcriptional, translational, and post-translational levels, resulting in the inhibition of the calcineurin–NFAT pathway, which resulted in the alteration of myofilament protein expression and sarcomere derangement in atrial tissues. These findings may help explain atrial myopathy in MetS. We suggest a therapeutic target on VLDLs to prevent atrial fibrillation, especially for individuals with MetS.

Sign in / Sign up

Export Citation Format

Share Document