L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

2018 ◽  
Vol 74 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Joanna J. Samulak ◽  
Angelika K. Sawicka ◽  
Dace Hartmane ◽  
Solveiga Grinberga ◽  
Osvalds Pugovics ◽  
...  
Keyword(s):  
Lipid Profile ◽  
Adhesion Molecule ◽  
Serum Proteins ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Intercellular Adhesion Molecule ◽  
Carnitine Supplementation ◽  
Intercellular Adhesion Molecule 1 ◽  
Factor Α

Background: L-carnitine can be metabolized to trimethylamine N-oxide (TMAO), a molecule that promotes atherogenesis through its interaction with macrophages and lipid metabolism. Objective: The aim of the present study was to assess whether L-carnitine supplementation may promote changes in selected serum biomarkers of atherosclerosis. Methods: Before the start, in the mid-point and after completing the 24-weeks supplementation protocol, fasting blood samples were taken from the antecubital vein. Plasma free L-carnitine and TMAO were determined by the UPLC/MS/MS method. Serum proteins were determined by the enzyme immunoassay method using commercially available kits. Total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, and triglycerides have been determined using standard automatic analyzer. Results: L-carnitine supplementation elevated fasting plasma carnitine in the mid-point of our study and it remained increased until the end of supplementation period. Moreover, it induced tenfold increase in plasma TMAO concentration but did not affect serum C-reactive protein, interleukin-6, tumour necrosis factor-α, L-selectin, P-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1 or lipid profile markers. Conclusion: We demonstrated that ­although oral L-carnitine supplementation significantly ­increased plasma TMAO concentration, no lipid profile changes or other markers of adverse cardiovascular events were detected in healthy aged women over the period of 24 weeks.

scholarly journals A allele of ICAM-1 rs5498 and VCAM-1 rs3181092 is correlated with increased risk for periodontal disease

2019 ◽  
Vol 14 (1) ◽  
pp. 638-646
Author(s):  
Qijun Sun ◽  
Zongxin Zhang ◽  
Yuejian Ou
Keyword(s):  
Periodontal Disease ◽  
Adhesion Molecule ◽  
High Performance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Intercellular Adhesion Molecule ◽  
Genotype Distribution ◽  
Intercellular Adhesion Molecule 1 ◽  
Protein Levels ◽  
Increased Risk

AbstractObjectivePeriodontal disease (PD) is viewed today as multifactorial problems initiated and sustained by bacteria but significantly modified by the body’s response to bacterial plaque. Recent studies have suggested that gene polymorphisms could be involved in the pathophysiology of periodontitis. This study aimed to investigate a possible correlation of the polymorphisms of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) with PD.MethodsThe genotypes of ICAM-1 and VCAM-1 were initially determined in PD patients using denaturing high performance liquid chromatography (DHPLC). ELISA was then conducted to measure ICAM-1 and VCAM-1 protein levels. Next, the association of ICAM-1/VCAM-1 genotype distribution and expression with clinical indicators and severity of PD was analyzed.ResultsPD patients contained increased levels of hemoglobin A1c (HbA1c), total cholesterol (TC), triglyceride (TG), and low-density lipoprotein (LDL), increased ICAM-1 and VCAM-1 protein levels, and decreased high-density lipoprotein (HDL) level. The GG genotype and G allele at ICAM-1 rs5498, as well as the AG and GG genotypes and G allele at VCAM-1 rs3181092 may reduce PD risk.ConclusionTo sum up, the overexpressed ICAM-1 and VCA M-1 as well as A allele of ICAM-1 rs5498 and VCAM-1 rs3181092 is associated with the onset of PD.

Levels of adhesion molecules do not decrease after 3 months of statin therapy in moderate hypercholesterolaemia

2003 ◽  
Vol 104 (2) ◽  
pp. 189-193 ◽  
Author(s):  
Bernd JILMA ◽  
Christian JOUKHADAR ◽  
Ulla DERHASCHNIG ◽  
Fausi RASSOUL ◽  
Volker RICHTER ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Plasma Levels ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Protein Levels ◽  
Cholesterol Levels ◽  
Before And After

Studies in animals and humans indicate a pivotal role for adhesion molecules (AMs) in the pathogenesis of atherosclerosis. Whereas an association between hypercholesterolaemia and AM expression has been suggested, it is unclear whether lowering cholesterol decreases AM expression and release. We compared the effects of a 3-month treatment with standard doses of three different statins (atorvastatin, simvastatin and pravastatin) on plasma levels of circulating AM (cAM) in 75 hypercholesterolaemic patients in a randomized clinical trial. Plasma levels of circulating (c)E-selectin, circulating intercellular adhesion molecule-1 (cICAM-1) and circulating vascular cell adhesion molecule-1 (cVCAM-1) were measured before and after 3 months of therapy. None of the statins lowered plasma cAM levels and pooled analyses of all patients showed a 1.7% [95% confidence interval (CI), -1.4–4.9%] increase in cE-selectin, a 2.1% (95% CI, -0.2–4.4%) increase in cICAM-1, and a 2.7% (95% CI, -0.6–6.1%) increase in cVCAM-1 levels. cAM levels did not decrease, even in patients with a >50% decrease (n = 19) in low-density lipoprotein cholesterol levels. This study provides strong evidence that 3 months of therapy with three different statins does not decrease cAM levels, despite normalization of cholesterol levels, and a minor decrease in C-reactive protein levels in patients with moderate hypercholesterolaemia.

scholarly journals Oxidized low-density lipoprotein-induced microparticles promote endothelial monocyte adhesion via intercellular adhesion molecule 1

2017 ◽  
Vol 313 (5) ◽  
pp. C567-C574 ◽  
Author(s):  
Zhiwei Fu ◽  
Enchen Zhou ◽  
Xu Wang ◽  
Mingda Tian ◽  
Jian Kong ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Adhesion Assay ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Intercellular Adhesion Molecule 1

Oxidized low-density lipoprotein (oxLDL) accumulates early in atherosclerotic lesions and plays an important role in the progressive formation of atherosclerotic plaques. Endothelial derived microparticles (EMPs) form a heterogeneous population of <1-μm particles that shed from endothelial membranes upon activation. While EMPs are shown to be involved in atherosclerotic pathophysiology and progression, there is no report regarding the relationship between oxLDL and EMPs. In this study, we aim to determine the influence of oxLDL on endothelial microparticle release and the subsequent regulation of the endothelial activation. EMPs were collected from the medium of human umbilical vein endothelial cells (HUVECs) treated with oxLDL or PBS as control. We find that oxLDL increases the release of EMPs containing intercellular adhesion molecule 1 (ICAM-1) but not vascular cell adhesion molecule 1 (VCAM-1). Confocal microscopy analysis further demonstrates that these EMPs interact with endothelial cells and increase the expression of ICAM-1 in HUVECs. The fact that injecting oxLDL-induced EMPs via the tail vein of ICR mice augments ICAM-1 expression on aortic endothelial cells confirms our results in vivo. Finally, oxLDL-induced EMPs from HUVECs increase the adhesion of monocytes to endothelial cells as determined by the adhesion assay. Our study suggests that oxLDL may augment the release of EMPs harboring increased levels of ICAM-1 that can be transferred to endothelial cells elsewhere. This leads to increased monocyte recruitment in other regions where oxLDL accumulation was initially more limited. EMPs may therefore serve as the mediator that propagates oxLDL-induced endothelial inflammation.

The effects of green tea ingestion over four weeks on atherosclerotic markers

2005 ◽  
Vol 42 (4) ◽  
pp. 292-297 ◽  
Author(s):  
Heungsup Sung ◽  
Won-Ki Min ◽  
Woochang Lee ◽  
Sail Chun ◽  
Hyosoon Park ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Lipid Profile ◽  
Green Tea ◽  
Adhesion Molecule ◽  
Biological Markers ◽  
Density Lipoprotein ◽  
Intercellular Adhesion Molecule ◽  
Rank Test ◽  
Intercellular Adhesion Molecule 1

Background: The objective of this study was to evaluate the effects of green tea ingestion over four weeks on atherosclerotic biological markers. Methods: After a one-week baseline period, 12 healthy male volunteers aged 28-42 years drank 600 mL of green tea dailyfor four weeks. Lipid profile, oxidized low-density lipoprotein (ox-LDL), total antioxidant capacity (TAC), C-reactive protein (CRP) and soluble cell adhesion molecules were measured at baseline and after two and four weeks ingestion of green tea. Results: There was no significantchange in the concentrations of lipid profile, TAC, CRP, soluble intercellular adhesion molecule-1 (sICAM-1), or soluble E-selectin after ingestion of green tea. The levels of ox-LDL and soluble vascular cell adhesion molecule-1 (sVCAM-1) were significantly decreased after four weeks of green tea ingestion (Wilcoxon signed rank test, P=0.006). Conclusions: The results of this study suggest an in vivo anti-oxidative effect for green tea and an influence of green tea on atherosclerotic biological markers. The effect of green tea seen on ox-LDL and sVCAM-1provides a potential mechanism for the cardiovascular benefits of regular ingestion of green tea.

scholarly journals Comparative effects of ethanol leaf and stem bark extracts of Irvingia gabonensis (BUSH MANGO) on sodium arsenite-induced lipid profile perturbtions in wistar rats

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Efosa Godwin Ewere ◽  
Ngozi Paulinus Okolie ◽  
Erhunmwunsee Dalton Avan ◽  
Patience Edet Umoh
Keyword(s):  
Lipid Profile ◽  
Wistar Rats ◽  
Sodium Arsenite ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Stem Bark ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Irvingia Gabonensis

Abstract Background Exposure to arsenic orchestrates a myriad of noxious health effects, including cancer. Different parts of Irvingia gabonensis are used as herbal remedies in traditional medicine. In this study, the comparative effects of the ethanol leaf (ELEIG) and stem bark extracts (ESEIG) of Irvingia gabonensis on sodium arsenite (SA)-induced lipid profile disturbances in Wistar rats were investigated. Methods Fifty five Wistar rats weighing between 100 g and 179 g were distributed into eleven groups (n=5). Group 1 (control) received feed and water ad libitum. Group 2 received SA at a dose of 4.1 mg/kg body weight (kgbw) for 14 days. Groups 3–11 were treated with the extracts with or without SA. Treatment was done by oral intubation for 14 days. Serum concentrations of total cholesterol (TC), triacylglycerol (TAG), high density lipoprotein cholesterol (HDL-c), low density lipoprotein cholesterol (LDL-c), very low density lipoprotein cholesterol (VLDL-c), total lipids (TL) and atherogenic index of plasma (AIP) were used to determine the lipid profile effects of the extracts. Results Exposure to SA caused significant (p ˂ 0.05) increases in all assayed parameters, relative to control. Post-treatment and simultaneous treatment with ELEIG and ESEIG mitigated the effects of SA. In addition, ELEIG alone at various doses produced results comparable with control values. However, ESEIG alone caused significant (p ˂ 0.05) increases in all assayed parameters, relative to control. Conclusion These results show that ELEIG and ESEIG ameliorate SA-induced lipid profile disturbances in Wistar rats. However, long-term administration of ESEIG alone may be discouraged.

Effect of Hydroxychloroquine on the Lipid Profile of Patients with Sjögren Syndrome

2014 ◽  
Vol 41 (5) ◽  
pp. 902-908 ◽  
Author(s):  
Michail P. Migkos ◽  
Theodora E. Markatseli ◽  
Chrisoula Iliou ◽  
Paraskevi V. Voulgari ◽  
Alexandros A. Drosos
Keyword(s):  
Lipid Profile ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Sjögren Syndrome ◽  
Lipoprotein Cholesterol ◽  
Atherogenic Index ◽  
Entire Group ◽  
Sjogren Syndrome ◽  
Significant Difference ◽  
Changes Over Time

Objective.Many studies have highlighted the hypolipidemic action of hydroxychloroquine (HCQ). We investigated the effect of HCQ on the lipid profile of patients with Sjögren syndrome (SS).Methods.The present retrospective observational study included 71 female patients with SS treated with HCQ. The levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol, triglycerides (TG), and atherogenic index (TC/HDL) were measured at baseline, after 6 months, and 1, 3, and 5 years after initiation of HCQ treatment. Analysis to investigate changes over time was performed in the entire patient group and in the separate subgroups: those receiving (21 patients) and those not receiving (50 patients) hypolipidemic treatment.Results.For the entire group of patients a statistically significant decrease in TC was noted (levels before treatment 220 ± 41 mg/dl, and at 5 yrs 206 ± 32 mg/dl, p = 0.006). A statistically significant difference was observed in the levels of HDL (57 ± 14 mg/dl vs 67 ± 17 mg/dl, p < 0.001) and in atherogenic index (4.0 ± 1.3 vs 3.3 ± 0.9, p < 0.001). Patients not receiving a hypolipidemic agent during the same period demonstrated a decrease in TC (214 ± 40 mg/dl vs 208 ± 34 mg/dl, p = 0.049), an increase in HDL levels (55 ± 15 mg/dl vs 67 ± 18 mg/dl, p < 0.001), and a decrease in atherogenic index (4.0 ± 1.4 vs 3.3 ± 0.9, p < 0.001). In the subgroup of patients receiving hypolipidemic treatment, the respective changes in their lipid profile were not significant in the first years but became significant in the long term.Conclusion.Use of HCQ in patients with SS was related to a statistically significant decrease in TC, an increase in HDL, and improvement in the atherogenic index.

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