scholarly journals TM6SF2 may drive postprandial lipoprotein cholesterol toxicity away from the vessel walls to the liver in NAFLD

2016 ◽  
Vol 64 (4) ◽  
pp. 979-981 ◽  
Author(s):  
Giovanni Musso ◽  
Maurizio Cassader ◽  
Elena Paschetta ◽  
Roberto Gambino
Keyword(s):  
Lipoprotein Cholesterol ◽  
Postprandial Lipoprotein ◽  
Vessel Walls

scholarly journals Atorvastatin Improves Postprandial Lipoprotein Metabolism in Normolipidemic Subjects1

2000 ◽  
Vol 85 (11) ◽  
pp. 4224-4230
Author(s):  
Klaus G. Parhofer ◽  
P. Hugh R. Barrett ◽  
Peter Schwandt
Keyword(s):  
High Density Lipoprotein ◽  
High Density Lipoprotein Cholesterol ◽  
Apolipoprotein B ◽  
Ldl Cholesterol ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Retinyl Palmitate ◽  
Lipoprotein Cholesterol ◽  
Atorvastatin Therapy ◽  
Postprandial Lipoprotein

Atorvastatin is a potent HMG-CoA reductase inhibitor that decreases low-density lipoprotein (LDL) cholesterol and fasting triglyceride concentrations. Because of the positive association between elevated postprandial lipoproteins and atherosclerosis, we investigated the effect of atorvastatin on postprandial lipoprotein metabolism. The effect of 4 weeks of atorvastatin therapy (10 mg/day) was evaluated in 10 normolipidemic men (30 ± 2 yr; body mass index, 22 ± 3 kg/m2; cholesterol, 4.84 ± 0.54 mmol/L; triglyceride, 1.47 ± 0.50 mmol/L; high-density lipoprotein cholesterol, 1.17 ± 0.18 mmol/L; LDL-cholesterol, 3.00 ± 0.49 mmol/L). Postprandial lipoprotein metabolism was evaluated with a standardized fat load (1300 kcal, 87% fat, 7% carbohydrates, 6% protein, 80,000 IU vitamin A) given after 12 h fast. Plasma was obtained every 2 h for 14 h. A chylomicron (CM) and a chylomicron-remnant (CR) fraction was isolated by ultracentrifugation, and triglycerides, cholesterol, apolipoprotein B, apoB-48, and retinyl-palmitate were determined in plasma and in each lipoprotein fraction. Atorvastatin therapy significantly (P < 0.001) decreased fasting cholesterol (−28%), triglycerides (−30%), LDL- cholesterol (-41%), and apolipoprotein B (−39%), whereas high-density lipoprotein cholesterol increased (4%, not significant). The area under the curve for plasma triglycerides (−27%) and CR triglycerides (−40%), cholesterol (−49%), and apoB-48 (−43%) decreased significantly (P < 0.05), whereas CR retinyl-palmitate decreased (−34%) with borderline significance (P = 0.08). However, none of the CM parameters changed with atorvastatin therapy. This indicates that, in addition to improving fasting lipoprotein concentrations, atorvastatin improves postprandial lipoprotein metabolism presumably by increasing CR clearance or by decreasing the conversion of CMs to CRs, thus increasing the direct removal of CMs from plasma.

Determination of fasting and postprandial lipoprotein cholesterol concentrations in pigs: A comparison of methods

2000 ◽  
Vol 20 (11) ◽  
pp. 1623-1631 ◽  
Author(s):  
Frazer J Allan ◽  
Roger N Johnson ◽  
Prudence V. McNutt ◽  
Kerry A.C. James ◽  
Keith G. Thompson ◽  
...  
Keyword(s):  
Lipoprotein Cholesterol ◽  
Comparison Of Methods ◽  
Postprandial Lipoprotein

Triglyceride to high density lipoprotein cholesterol ratio, total cholesterol to high density lipoprotein cholesterol ratio and low ankle brachial index in an elderly population

VASA ◽  
2014 ◽  
Vol 43 (3) ◽  
pp. 189-197 ◽  
Author(s):  
Yiqiang Zhan ◽  
Jinming Yu ◽  
Rongjing Ding ◽  
Yihong Sun ◽  
Dayi Hu
Keyword(s):  
High Density Lipoprotein ◽  
Total Cholesterol ◽  
High Density Lipoprotein Cholesterol ◽  
Ankle Brachial Index ◽  
Density Lipoprotein ◽  
High Density ◽  
Lipoprotein Cholesterol ◽  
Lipid Lowering ◽  
Cholesterol Ratio ◽  
Potential Biomarker

Background: The associations of triglyceride (TG) to high-density lipoprotein cholesterol ratio (HDL‑C) and total cholesterol (TC) to HDL‑C ratio and low ankle brachial index (ABI) were seldom investigated. Patients and methods: A population based cross-sectional survey was conducted and 2982 participants 60 years and over were recruited. TG, TC, HDL‑C, and low-density lipoprotein cholesterol (LDL-C) were assessed in all participants. Low ABI was defined as ABI ≤ 0.9 in either leg. Multiple logistic regression models were applied to study the association between TG/HDL‑C ratio, TC/HDL‑C ratio and low ABI. Results: The TG/HDL‑C ratios for those with ABI > 0.9 and ABI ≤ 0.9 were 1.28 ± 1.20 and 1.48 ± 1.13 (P < 0.0001), while the TC/HDL‑C ratios were 3.96 ± 1.09 and 4.32 ± 1.15 (P < 0.0001), respectively. After adjusting for age, gender, body mass index, obesity, current drinking, physical activity, hypertension, diabetes, lipid-lowering drugs, and cardiovascular disease history, the odds ratios (ORs) with 95 % confidence intervals (CIs) of low ABI for TG/HDL‑C ratio and TC/HDL‑C ratio were 1.10 (0.96, 1.26) and 1.34 (1.14, 1.59) in non-smokers. When TC was further adjusted, the ORs (95 % CIs) were 1.40 (0.79, 2.52) and 1.53 (1.21, 1.93) for TG/HDL‑C ratio and TC/HDL‑C ratio, respectively. Non-linear relationships were detected between TG/HDL‑C ratio and TC/HDL‑C ratio and low ABI in both smokers and non-smokers. Conclusions: TC/HDL‑C ratio was significantly associated with low ABI in non-smokers and the association was independent of TC, TG, HDL‑C, and LDL-C. TC/HDL‑C might be considered as a potential biomarker for early peripheral arterial disease screening.

Plasminogen Activator Inhibitor-1 Expression in Human Liver and Healthy or Atherosclerotic Vessel Walls

1994 ◽  
Vol 72 (01) ◽  
pp. 044-053 ◽  
Author(s):  
N Chomiki ◽  
M Henry ◽  
M C Alessi ◽  
F Anfosso ◽  
I Juhan-Vague
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Plasminogen Activator ◽  
Human Liver ◽  
Plasminogen Activator Inhibitor ◽  
Muscle Cells ◽  
Vessel Walls ◽  
Activator Inhibitor ◽  
Pai 1

SummaryIndividuals with elevated levels of plasminogen activator inhibitor type 1 are at risk of developing atherosclerosis. The mechanisms leading to increased plasma PAI-1 concentrations are not well understood. The link observed between increased PAI-1 levels and insulin resistance has lead workers to investigate the effects of insulin or triglyceride rich lipoproteins on PAI-1 production by cultured hepatocytes or endothelial cells. However, little is known about the contribution of these cells to PAI-1 production in vivo. We have studied the expression of PAI-1 in human liver sections as well as in vessel walls from different territories, by immunocytochemistry and in situ hybridization.We have observed that normal liver endothelial cells expressed PAI-1 while parenchymal cells did not. However, this fact does not refute the role of parenchymal liver cells in pathological states.In healthy vessels, PAI-1 mRNA and protein were detected primarily at the endothelium from the lumen as well as from the vasa vasorum. In normal arteries, smooth muscle cells were able to produce PAI-1 depending on the territory tested. In deeply altered vessels, PAI-1 expression was observed in neovessels scattering the lesions, in some intimal cells and in smooth muscle cells. Local increase PAI-1 mRNA described in atherosclerotic lesions could be due to the abundant neovascularization present in the lesion as well as a raised expression in smooth muscle cells. The increased PAI-1 in atherosclerosis could lead to fibrin deposit during plaque rupture contributing further to the development and progression of the lesion.

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