Low Density Lipoprotein
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Chinenye E. Oguazu ◽  
Francis C. Ezeonu ◽  
Charles C. Dike ◽  
Charles G. Ikimi

Background and Objectives: Living organisms are exposed to oxidant agents constantly from both endogenous and exogenous sources. One of such oxidant agent is Bisphenol A (BPA) and its exposure is capable to modify biomolecules and induce damages. Bisphenol A (BPA) is a contaminant with increasing exposure. It exerts toxic effects on cells.  This study investigates the possibility of BPA exposure on Low Density Lipoprotein (LDL) perturbations at prevailing low exposure doses in female albino Wistar rats, following exposure for the period of three (3) month. Materials and Methods: Total 12 groups were formed; out of which 11 experimental groups, each containing 10non-pregnant female rats were administered; 0.05, 0.1, 0.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, and 1 mg of BPA/kgbw/day. To the 12th control group was given water.  Blood was collected from animals at the end of every week of the study and serum sample specimens analyzed by routine diagnostic procedures for oxidized LDL such as malondialdehyde modified- LDL (MDA-LDL), oxidized phospholipids LDL (OX-PL LDL), N (epsilon) (carboxymethyl) lysine-modified-LDL (CML LDL) and 4-hydroxynonenal-LDL (HNE-LDL) using Autochemical Analyzer. Results: Significantly increased concentrations of serum oxidized LDL such as MDA-LDL, OX-PL LDL, CML LDL and HNE-LDL were observed at all concentrations of BPA exposure. Conclusion:  Bisphenol A alters oxidized LDL such as MDA-LDL, OX-PL LDL, CML LDL and HNE-LDL balance and causes disturbance of internal oxidative statues.

2021 ◽  
Vol 26 (3S) ◽  
pp. 4610
O. P. Ishevskaia ◽  
A. M. Namitokov ◽  
S. V. Kruchinova ◽  
E. D. Kosmacheva

Introduction. Cardiovascular events at a young age are often the first manifestation of a genetic disorder such as familial hypercholesterolemia. High cholesterol levels, xanthomas and xanthelasmas, as well as a positive family history of cardiovascular disease, make it possible to identify a group of patients subject to genetic research. The identification of a specific mutation helps to determine further strategy not only for a patient, but also to his or her immediate relatives, thereby effectively conducting both secondary and primary prevention of atherosclerosis complications.Brief description. Using the example of patients from the Krasnodar Lipid Center, the relevance of genetic testing and cascade screening is demonstrated. We show problems of delayed diagnosis and low medical adherence, as well as the ways to optimize care for patients with genetic lipid metabolism disorders.Discussion. The rise in the incidence of cardiovascular events at a young age in developed countries prompts the search for more improved screening and diagnostic methods for familial hypercholesterolemia. The optimal age of initiation of lipid-lowering therapy in children with established familial hypercholesterolemia is also discussed. While secondary prevention appears to be clearer, there is still insufficient achievement of low-density lipoprotein cholesterol targets in patients with a previous cardiovascular event.

2021 ◽  
Vol 11 (1) ◽  
Amra Jujić ◽  
J. Korduner ◽  
H. Holm ◽  
G. Engström ◽  
E. Bachus ◽  

AbstractObesity associates with reduced life expectancy, type 2 diabetes, hypertension and cardiovascular disease, and is characterized by chronic inflammation. Phosphorylcholine (PC) is an epitope on oxidized low-density lipoprotein, dead cells and some microorganisms. Antibodies against PC (anti-PC) have anti-inflammatory properties. Here, we explored the role of anti-PC in hospitalized versus non-hospitalized obese. One-hundred-and-twenty-eight obese (BMI ≥ 30 kg/m2) individuals (59.8 (± 5.5) years, 53.9% women) from the Malmö Diet and Cancer Cardiovascular Cohort were examined and IgM, IgG1 and IgG2 anti-PC were analyzed by ELISA. Individuals with at least one recorded history of hospitalization prior to study baseline were considered hospitalized obese (HO). Associations between IgM, IgG1 and IgG2 anti-PC and HO (n = 32)/non-hospitalized obese (NHO) (n = 96), but also with metabolic syndrome and diabetes were analysed using logistic regressions. Both IgM and IgG1 anti-PC were inversely associated with HO, also after controlling for age and sex. When further adjusted for waist circumference, systolic blood pressure, glucose levels and smoking status, only IgG1 anti-PC remained significantly associated with HO. In multivariate models, each 1 standard deviation of increment in anti-PC IgG1 levels was inversely associated with prevalence of HO (odds ratio 0.57; CI 95% 0.33–0.98; p = 0.044). IgG2 anti-PC did not show any associations with HO. Low levels of IgM and IgG1 anti-PC are associated with higher risk of being a HO individual independent of sex and age, IgG1 anti-PC also independently of diabetes and metabolic syndrome. The anti-inflammatory properties of these antibodies may be related to inflammation in obesity and its complications.

2021 ◽  
Vol 8 ◽  
Xiao Li ◽  
Xihe Tang ◽  
Bo Liu ◽  
Jinghang Zhang ◽  
Yongxi Zhang ◽  

Background: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a transmembrane glycoprotein that mediates uptake of oxidized low-density lipoprotein (ox-LDL) into cells. Previous studies had shown that LOX-1 deletion had a potential to inhibit cardiac fibrosis in mouse models of hypertension and myocardial infarction. Whether LOX-1 deletion also affects cardiac fibrosis associated with aging still remains unknown. The aim of this study was to investigate the effect of LOX-1 deletion on myocardial fibrosis in the aged mice.Methods: C57BL/6 mice and LOX-1 knockout (KO) mice with C57BL/6 background were studied to the age of 60 weeks. Both genotypes of aged mice were exposed to angiotensin II (Ang II) or saline for additional 4 weeks. The mice were then sacrificed, and myocardial fibrosis, reactive oxygen species (ROS) and expression of LOX-1, fibronectin, collagens, p22phox, and gp91phox were measured.Results: LOX-1 deletion markedly reduced Ang II-mediated rise of blood pressure in the aged mice (vs. saline-treated mice). LOX-1 deletion also limited fibrosis and decreased fibronectin and collagen-3 expression in the hearts of aged mice, but not the expression of collagen-1 and collagen-4. LOX-1 deletion also inhibited ROS production and p22phox expression. As the aged mice were exposed to Ang II for 4 weeks (resulting in hypertension), LOX-1 deletion more pronounced inhibiting myocardial fibrosis and ROS production, and decreasing expression of fibronectin, collagen-1, collagen-2, collagen-3, p22phox, and gp91phox.Conclusion: LOX-1 deletion limited fibrosis and ROS production in the hearts of aged mice. This effect was more pronounced in the aged mice with hypertension induced by Ang II infusion.

Genes ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 1599
Dana Dlouha ◽  
Milan Blaha ◽  
Eva Rohlova ◽  
Jaroslav A. Hubacek ◽  
Vera Lanska ◽  

Familial hypercholesterolemia (FH), is an autosomal dominant disorder caused by mutations in the LDLR, APOB, PCSK9, and APOE genes and is characterized by high plasma levels of total and low-density lipoprotein (LDL) cholesterol. Our study aimed to analyze the influences of two different therapies on a wide spectrum of plasma protein biomarkers of cardiovascular diseases. Plasma from FH patients under hypolipidemic therapy (N = 18; men = 8, age 55.4 ± 13.1 years) and patients under combined long-term LDL apheresis/hypolipidemic therapy (N = 14; men = 7; age 58.0 ± 13.6 years) were analyzed in our study. We measured a profile of 184 cardiovascular disease (CVD) associated proteins using a proximity extension assay (PEA). Hypolipidemic therapy significantly (all p < 0.01) influenced 10 plasma proteins (TM, DKK1, CCL3, CD4, PDGF subunit B, AGRP, IL18, THPO, and LOX1 decreased; ST2 increased). Under combined apheresis/hypolipidemic treatment, 18 plasma proteins (LDLR, PCSK9, MMP-3, GDF2, CTRC, SORT1, VEGFD, IL27, CCL24, and KIM1 decreased; OPN, COL1A1, KLK6, IL4RA, PLC, TNFR1, GLO1, and PTX3 increased) were significantly affected (all p < 0.006). Hypolipidemic treatment mainly affected biomarkers involved in vascular endothelial maintenance. Combined therapy influenced proteins that participate in cholesterol metabolism and inflammation.

2021 ◽  
Vol 11 (1) ◽  
Eka R. Gunardi ◽  
Raymond Surya ◽  
Inayah Syafitri ◽  
Yogi Pasidri

AbstractThe aim of this study was to investigate the effect of a one-rod levonorgestrel implant on the blood chemistry profile, including random blood glucose (RBG), haemoglobin (Hb), alanine transferase (ALT), aspartate transferase (AST), and the lipid profile, including total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and triglycerides. This prospective cohort study was conducted at Raden Saleh Clinic, Jakarta, from 2010 to 2012. The implants were inserted subdermally in 30 patients. The subjects were evaluated every 6 month up to 2 years. Bivariate analysis using t-test or Wilcoxon signed rank test was performed for all variables. p < 0.05 was considered a significant value. The Hb, RBG, AST, and lipid profile levels were significantly different before and 6 months after one-rod implant insertion (p < 0.05). However, for 24 months, all of the parameters were still within normal limits and did not differ clinically. One-rod levonorgestrel implant insertion has a minimal effect on all blood chemistry profiles.

2021 ◽  
Vol 41 (1) ◽  
pp. 333-361
Krista A. Varady ◽  
Sofia Cienfuegos ◽  
Mark Ezpeleta ◽  
Kelsey Gabel

This review aims to summarize the effects of intermittent fasting on markers of cardiometabolic health in humans. All forms of fasting reviewed here—alternate-day fasting (ADF), the 5:2 diet, and time-restricted eating (TRE)—produced mild to moderate weight loss (1–8% from baseline) and consistent reductions in energy intake (10–30% from baseline). These regimens may benefit cardiometabolic health by decreasing blood pressure, insulin resistance, and oxidative stress. Low-density lipoprotein cholesterol and triglyceride levels are also lowered, but findings are variable. Other health benefits, such as improved appetite regulation and favorable changes in the diversity of the gut microbiome, have also been demonstrated, but evidence for these effects is limited. Intermittent fasting is generally safe and does not result in energy level disturbances or increased disordered eating behaviors. In summary, intermittent fasting is a safe diet therapy that can produce clinically significant weight loss (>5%) and improve several markers of metabolic health in individuals with obesity.

C. Srinivasa ◽  
K. La Kshminarayan ◽  
V. Srinivas ◽  
B. V. S. Chandrasekhar

Background: Current treatment with statins has become an integral part of vascular diseases but monotherapy has a significant residual event rate. Due to particularly one of the factor associated with atherogenic lipid phenotype that is characterized by a low high-density lipoprotein (HDL) cholesterol and increase in non-HDL cholesterol like Low-Density Lipoprotein (LDL). Omega-3 Fatty acids have demonstrated a preventiverole in primary and, particularly secondary cardiovascular diseases.  Hence this study was planned to compare the efficacy of Atorvastatin alone with Atorvastatin and Omega-3 fatty acids in treatment in hyperlipidaemia patients. Methods: The study was comparative, randomized, and prospective and open labeled conducted in MI patients. A total of 100 patients were selected based on inclusion and exclusion criteria. They were divided randomly into two Groups (Group–A and Group-B). Group-A was given Atorvastatin 10mg/day and Group-B was given Atorvastatin 10mg/day and Omega-3 fatty acids 600mg/day for 6 months. Follow up was done every month and efficacy was measured by assessing the lipoprotein levels in serum. Results: The results were compared before treatment and after 6 months treatment.The levels were significantly decreased Total Cholesterol (TC), LDL, Low-Density Lipoprotein (VLDL), Triglycerides (TG) and HDL levels were increased in Group–A and Group-B. When these results compared between two Groups the HDL levels were increased also it shown high significance (<0.001) but there were no significance changes in other cholesterol levels. Conclusion: The present study results showed that Atorvastatin and Omega-3 fatty acids treatment was more effective than Atorvastatin alone treatment in improving HDL-C levels from base line and it may have a additive effect in major coronary artery diseases.

Mohamad Dandan ◽  
Julia Han ◽  
Sabrina Mann ◽  
Rachael Kim ◽  
Hussein Mohammed ◽  

Objective: We measured the turnover rates of the LDLR (low-density lipoprotein receptor) and PCSK9 (proprotein convertase subtilisin/kexin type 9) in mice by metabolic labeling with heavy water and mass spectrometry. Approach and Results: In liver of mice fed high-cholesterol diets, LDLR mRNA levels and synthesis rates were markedly lower with complete suppression of cholesterol synthesis and higher cholesterol content, consistent with the Brown-Goldstein model of tissue cholesterol homeostasis. We observed markedly lower PCSK9 mRNA levels and synthesis rates in liver and lower concentrations and synthesis rates in plasma. Hepatic LDLR half-life (t½) was prolonged, consistent with an effect of reduced PCSK9, and resulted in no reduction in hepatic LDLR content despite reduced mRNA levels and LDLR synthesis rates. These changes in PCSK9 synthesis complement and expand the well-established model of tissue cholesterol homeostasis in mouse liver, in that reduced synthesis and levels of PCSK9 counterbalance lower LDLR synthesis by promoting less LDLR catabolism, thereby maintaining uptake of LDL cholesterol into liver despite high intracellular cholesterol concentrations. Conclusions: Lower hepatic synthesis and secretion of PCSK9, an SREBP2 (sterol response element binding protein) target gene, results in longer hepatic LDLR t½ in response to cholesterol feeding in mice in the face of high intracellular cholesterol content. PCSK9 modulation opposes the canonical lowering of LDLR mRNA and synthesis by cholesterol surplus and preserves LDLR levels. The physiological and therapeutic implications of these opposing control mechanisms over liver LDLR are of interest and may reflect subservience of hepatic cholesterol homeostasis to whole body cholesterol needs.

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