scholarly journals Effects of cigarette smoke-modified low density lipoprotein (CS-LDL) on vascular reactivity and cholesterol accumulation in macrophages.

1994 ◽  
Vol 64 ◽  
pp. 269
Author(s):  
Satomi Kitagawa ◽  
Yu Yamaguchi ◽  
Emiko Sameshima ◽  
Masaru Kunitomo
Keyword(s):  
Cigarette Smoke ◽  
Vascular Reactivity ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Cholesterol Accumulation

scholarly journals Effect of cell density on binding and uptake of low density lipoprotein by human fibroblasts.

1979 ◽  
Vol 83 (3) ◽  
pp. 588-594 ◽  
Author(s):  
H S Kruth ◽  
J Avigan ◽  
W Gamble ◽  
M Vaughan
Keyword(s):  
Cell Density ◽  
Low Density Lipoprotein ◽  
Human Fibroblasts ◽  
Density Lipoprotein ◽  
Low Density ◽  
Cellular Lipid ◽  
Cholesterol Accumulation ◽  
Ldl Receptors ◽  
Ldl Binding ◽  
In Cells

The effect of cell density on low density lipoprotein (LDL) binding by cultured human skin fibroblasts was investigated. Bound LDL was visualized by indirect immunofluorescence. Cellular lipid and cholesterol were monitored by fluorescence in cells stained with phosphine 3R and filipin, respectively. LDL binding and lipid accumulation were compared in cells in stationary and exponentially growing cultures, in sparsely and densely plated cultures, in wounded and non-wounded areas of stationary cultures, and in stationary cultures with and without the addition of lipoprotein-deficient serum. We conclude that LDL binding and cholesterol accumulation induced by LDL are influenced by cell density. It appears that, compared to rapidly growing cells, quiescent (noncycling) human fibroblasts exhibit fewer functional LDL receptors.

Emodin alleviated hyperlipidemia and hepatic lipid metabolism in zebrafish larvae fed a high-cholesterol diet via AMPK/SREBP-2/PCSK9/LDLR signaling pathway

2021 ◽  
Author(s):  
Linfeng He ◽  
Cheng Wang ◽  
Yafang Zhang ◽  
Chaocheng Guo ◽  
Yan Wan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Cholesterol Diet ◽  
Low Density ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Cholesterol Accumulation ◽  
Hepatic Lipid ◽  
Zebrafish Larvae

Abstract BackgroundEmodin (EM) is one of bioactive components extracted from Rheum palmatum L. (Dahuang), which possesses numerous pharmacological activities including hypolipidemic effect. However, the potential action of EM on hyperlipidemia (HLP) remains unclear. Here, the theraputic effect of EM against HLP were investigated.MethodsIn this study, the hypolipidemic properties of EM were evaluated using high-cholesterol diet (HCD)-stimulated zebrafish larvae model. The body weight, body length and body mass index (BMI) was measured. The total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) as well as the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected by corresponding assay kits. Tg (flil: eGFP) zebrafish were utilized to observe vascular cholesterol accumulation and Tg (mpx: eGFP) zebrafish to visualize and quantify neutrophil inflammation. The hepatic lipid deposition and hepatic histopathology were analyzed by Oil red O staining and H&E staining, respectively. Finally, the underlying mechanism of EM were investigated using real-time quantitative PCR (RT-qPCR) analysis to assess the gene levels of adenosine monophosphate-activated protein kinase alpha (AMPKα), sterol regulatory element binding protein 2 (SREBP-2), proprotein convertase subtilisin kexin 9 (PCSK9), low-density lipoprotein receptor (LDLR), 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR), adenosine triphosphate binding cassette transporter A1 (ABCA1) and adenosine triphosphate binding cassette transporter G1 (ABCG1).ResultsOur data indicated that EM reduced obesity of zebrafish as evidenced by the decrease in body weight, body length and BMI. EM significantly reduced TC, TG, and LDL-C, and increased HDL-C contents. Moreover, it displayed a prominent inhibitory effect on blood cholesterol accumulation, hepatic lipid accumulation, and neutrophil inflammation in vascular site. Additionally, EM improved the liver function through decreasing ALT and AST levels of zebrafish with HCD-induced hepatosteatosis. Further investigation showed that EM treatment attenuated lipid accumulation via upregulating the expression of AMPKα, LDLR, ABCA1 and ABCG1, and downregulating the expression of SREBP-2, PCSK9 and HMGCR.ConclusionTo conclude, EM alleviated lipid metabolism disorder symptoms caused by HCD via modulating AMPK/SREBP-2/PCSK9/LDLR pathway in larvae, suggesting that EM may be developed into hypolipidmic agent for treating lipid metabolism related diseases.

scholarly journals The association of nadir CD4-T cell count and endothelial dysfunction in a healthy HIV cohort without major cardiovascular risk factors

2020 ◽  
Vol 8 ◽  
pp. 205031212092489
Author(s):  
Emad Mogadam ◽  
Kevin King ◽  
Kimberly Shriner ◽  
Karen Chu ◽  
Anders Sondergaard ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Vascular Reactivity ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Reactivity Index ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol

Objectives: HIV-infected population may have increased risk of cardiovascular disease. The prevalence of traditional cardiovascular disease risk factors such as hypertension, diabetes and dyslipidemia in HIV-infected individuals has made it difficult to assess the direct effects of HIV and immune factors on endothelial dysfunction and associated increased risk of atherosclerosis. The purpose of this study was to investigate indicators of endothelial dysfunction in an HIV cohort without hypertension and diabetes. Methods: We studied 19 HIV-infected patients between the ages of 25–76 years old with effectively suppressed viral load and without diagnosis of hypertension or diabetes. Endothelial function was measured by digital thermal monitoring of vascular reactivity using the VENDYS technique. Endothelial function was reported as vascular reactivity index. Systolic blood pressure and diastolic blood pressure at the time of VENDYS test were measured and latest lipid panels were recorded. The association between vascular reactivity index and CD4-T cells count, different antiretroviral therapy types (non-nucleoside reverse transcriptase, nucleoside reverse transcriptase, protease inhibitors, integrase inhibitors), vitamins use, systolic blood pressure, diastolic blood pressure, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol was investigated. Results: Mean vascular reactivity index was 1.87 ± 0.53. Vascular reactivity index, marker of endothelial dysfunction, showed a significant correlation with lower nadir CD4 count (p = 0.003) as well as low-density lipoprotein cholesterol (p = 0.02). No additional significant correlation between vascular reactivity index and the rest of the investigated variables was found. Conclusion: Vascular reactivity index, a clinical predictor of endothelial dysfunction, is associated with lower nadir CD4-T cell and low-density lipoprotein cholesterol in HIV-infected men with no history of hypertension or diabetes and before clinical evidence of cardiovascular disease.

Low-density lipoprotein cholesterol levels in adults with type 2 diabetes: An alternative equation for accurate estimation and improved cardiovascular risk classification

2014 ◽  
Vol 11 (6) ◽  
pp. 431-439 ◽  
Author(s):  
Ester Yeoh Chai Kheng ◽  
Sum Chee Fang ◽  
Su Chang ◽  
Serena Low Kiat Mun ◽  
Lim Su Chi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Vascular Reactivity ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Accurate Estimation ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Therapeutic Decisions

Low-density lipoprotein cholesterol (LDL-C) is a major risk factor for atherosclerotic disease. Despite its limitations, Friedewald-calculated LDL-C (F-LDL-C) remains widely used for LDL-C determination. In this observational study of 1999 adults with type 2 diabetes mellitus (T2DM), we compare the accuracy of F-LDL-C to directly measured LDL-C (M-LDL-C) and derived and validated a new [SMART2D (Singapore Study of MAcro-angiopathy and Micro-Vascular Reactivity in Type 2 Diabetes)] formula to estimate LDL-C. From 1000 randomly selected patients, M-LDL-C was compared to F-LDL-C. Using multiple linear regression to identify independent predictors for M-LDL-C, the SMART2D equation was derived and subsequently validated in the next 981 patients. F-LDL-C was 0.367 (0.216) mmol/L lower than M-LDL-C. This difference was −0.009 (0.189) for SMART2D-LDL-C. Using F-LDL-C, 27% with M-LDL-C ≥2.6 mmol/L were classified as LDL-C <2.6 mmol/L, reduced to 2.1% when using SMART2D-LDL-C. With F-LDL-C, misclassification was greater when triglycerides were ≥2.2 mmol/L, especially for the lower LDL-C cut-offs (1.8 and 2.6 mmol/L), and this was markedly improved with SMART2D-LDL-C. In conclusion, in T2DM, F-LDL-C underestimates M-LDL-C, with misclassifications that may potentially have an impact on therapeutic decisions in T2DM. The SMART2D equation improves accuracy of estimate, reducing misclassifications. Trials will be needed to ascertain the clinical significance of these findings.

Relationship between Vascular Reactivity and Lipids in Mexican-Americans with Type 2 Diabetes Treated with Pioglitazone

2007 ◽  
Vol 92 (4) ◽  
pp. 1256-1262 ◽  
Author(s):  
Estela Wajcberg ◽  
Apiradee Sriwijitkamol ◽  
Nicolas Musi ◽  
Ralph A. DeFronzo ◽  
Eugenio Cersosimo
Keyword(s):  
Type 2 Diabetes ◽  
Glycemic Control ◽  
Vascular Reactivity ◽  
Vascular Dysfunction ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Plasma Adiponectin ◽  
Lipoprotein Particle Size

Abstract Context: Vascular dysfunction and insulin resistance precede atherosclerosis in type 2 diabetes (T2DM). Better knowledge of the interaction between these is of considerable clinical interest. Objective: The objective of this study was to examine the association between inflammation, glucose, and lipid metabolism and vascular dysfunction. Design and Setting: We conducted a randomized, double-blind, controlled trial of pioglitazone vs. placebo and other therapies aimed at equal glycemic control for 24 wk at an academic tertiary referral clinic. Patients and Interventions: Mexican-American subjects with T2DM and no complications were randomly assigned to pioglitazone 45 mg daily (PIO, n = 16) or placebo (CON, n = 15) and matched for age, gender, body mass index, diabetes duration, and glycemic control. All subjects completed the study. Main Outcome Measure: We looked for improved vascular reactivity independent of glycemic control but closely related to plasma adiponectin, lipids, and insulin sensitivity. Results: After 24 wk, there was an equal decrease in fasting plasma glucose (∼135 mg/dl), glycosylated hemoglobin (∼7.0%), and glucose production (∼15%). The decrease in free fatty acids (30 vs. 10%) and increase in glucose disposal (40 vs. 25%) were greater in PIO vs. CON (P &lt; 0.05). In PIO, plasma high-density lipoprotein rose by 15% (P &lt; 0.05), and low-density lipoprotein and high-density lipoprotein particle size rose significantly (P &lt; 0.01). Plasma adiponectin doubled in PIO (from 6.1 ± 0.8 to 12.7 ± 2.1 μg/ml). Forearm blood flow rose equally (∼130%) during reactive hyperemia in both groups, although after therapy, the increase was greater (P &lt; 0.001) in PIO (153%) than in CON (137%); vasodilation was greater (P = 0.01) in PIO (92, 160, and 204%) than in CON with acetylcholine (74, 130, and 144%) and with sodium nitroprusside (PIO = 164 and 253% vs. 116 and 230%; P = 0.04). The elevation in diameter was also greater in PIO (13 vs. 10%; P &lt; 0.05). Vascular responses correlated with plasma free fatty acids, adiponectin, and low-density lipoprotein particle size but not with glycemic control. Conclusion: These data indicate that pioglitazone improves vascular reactivity irrespective of glycemic control and suggest a close association with changes in fat cell metabolism.

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