Naringin Time-Dependently Lowers Hepatic Cholesterol Biosynthesis and Plasma Cholesterol in Rats Fed High-Fat and High-Cholesterol Diet

2006 ◽  
Vol 9 (4) ◽  
pp. 582-586 ◽  
Author(s):  
So-Yeon Kim ◽  
Hye-Jin Kim ◽  
Mi-Kyung Lee ◽  
Seon-Min Jeon ◽  
Gyeong-Min Do ◽  
...  
Keyword(s):  
Plasma Cholesterol ◽  
Cholesterol Biosynthesis ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
Hepatic Cholesterol ◽  
High Cholesterol ◽  
High Fat

scholarly journals Phosphatidylcholine transfer protein regulates size and hepatic uptake of high-density lipoproteins

2005 ◽  
Vol 289 (6) ◽  
pp. G1067-G1074 ◽  
Author(s):  
Michele K. Wu ◽  
David E. Cohen
Keyword(s):  
Plasma Cholesterol ◽  
High Cholesterol Diet ◽  
Atp Binding ◽  
Cholesterol Diet ◽  
Wild Type ◽  
High Cholesterol ◽  
High Fat ◽  
Transfer Protein ◽  
Phosphatidylcholine Transfer Protein ◽  
Atp Binding Cassette

Phosphatidylcholine transfer protein (PC-TP) is a steroidogenic acute regulatory-related transfer domain protein that is enriched in liver cytosol and binds phosphatidylcholines with high specificity. In tissue culture systems, PC-TP promotes ATP-binding cassette protein A1-mediated efflux of cholesterol and phosphatidylcholine molecules as nascent pre-β-high-density lipoprotein (HDL) particles. Here, we explored a role for PC-TP in HDL metabolism in vivo utilizing 8-wk-old male Pctp−/− and wild-type littermate C57BL/6J mice that were fed for 7 days with either chow or a high-fat/high-cholesterol diet. In chow-fed mice, neither plasma cholesterol concentrations nor the concentrations and compositions of plasma phospholipids were influenced by PC-TP expression. However, in Pctp−/− mice, there was an accumulation of small α-migrating HDL particles. This occurred without changes in hepatic expression of ATP-binding cassette protein A1 or in proteins that regulate the intravascular metabolism and clearance of HDL particles. In Pctp−/− mice fed the high-fat/high-cholesterol diet, HDL particle sizes were normalized, whereas plasma cholesterol and phospholipid concentrations were increased compared with wild-type mice. In the absence of upregulation of hepatic ATP-binding cassette protein A1, reduced HDL uptake from plasma into livers of Pctp−/− mice contributed to higher plasma lipid concentrations. These data indicate that PC-TP is not essential for the enrichment of HDL with phosphatidylcholines but that it does modulate particle size and rates of hepatic clearance.

scholarly journals Trimethylamine N-oxide attenuates high-fat high-cholesterol diet-induced steatohepatitis by reducing hepatic cholesterol overload in rats

2019 ◽  
Vol 25 (20) ◽  
pp. 2450-2462 ◽  
Author(s):  
Ze-Hua Zhao ◽  
Feng-Zhi Xin ◽  
Da Zhou ◽  
Ya-Qian Xue ◽  
Xiao-Lin Liu ◽  
...  
Keyword(s):  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
Hepatic Cholesterol ◽  
High Cholesterol ◽  
High Fat

Sub-chronic microcystin-LR renal toxicity in rats fed a high fat/high cholesterol diet

Chemosphere ◽  
2020 ◽  
pp. 128773
Author(s):  
Tarana Arman ◽  
Katherine D. Lynch ◽  
Michael Goedken ◽  
John D. Clarke
Keyword(s):  
Renal Toxicity ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat

scholarly journals Interleukin-18 predicts atherosclerosis progression in SIV-infected and uninfected rhesus monkeys (Macaca mulatta) on a high-fat/high-cholesterol diet

2009 ◽  
Vol 89 (6) ◽  
pp. 657-667 ◽  
Author(s):  
Jennifer H Yearley ◽  
Dongling Xia ◽  
Christine B Pearson ◽  
Angela Carville ◽  
Richard P Shannon ◽  
...  
Keyword(s):  
Macaca Mulatta ◽  
Rhesus Monkeys ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
Interleukin 18 ◽  
High Cholesterol ◽  
High Fat ◽  
Atherosclerosis Progression

Abstract 130: Hypercholesterolemia Suppresses Carotid Artery Endothelial NOS3 Expression via Epigenetic Mechanisms

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Alex Sotolongo ◽  
Yi-Zhou Jiang ◽  
John Karanian ◽  
William Pritchard ◽  
Peter Davies
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Endothelial Cells ◽  
Dna Methyltransferase ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat

Objective: One of the first clinically detectable changes in the vasculature during atherogenesis is the accumulation of cholesterol within the vessel wall. Hypercholesterolemia is characterized by dysfunctional endothelial-dependent vessel relaxation and impaired NOS3 function. Since DNA methylation at gene promoter regions strongly suppresses gene expression, we postulated that high-fat/high-cholesterol diet suppresses endothelial NOS3 through promoter DNA methylation. Methods: Domestic male pigs were fed control diet (CD) or isocaloric high fat and high cholesterol diet (HC; 12% fat and 1.5% cholesterol) for 2, 4, 8 or 12 weeks prior to tissue collection. Furthermore, to determine the effects of risk factor withdrawal, an additional group of swine received HC for 12 weeks and then CD for 8 weeks; a control group received HC continuously for 20 weeks. Endothelial cells were harvested from common carotid aorta. In parallel in vitro studies, cultured human aortic endothelial cells (HAEC) were treated with human LDL, GW3956 (LXR agonist) and RG108 (DNA methyltransferase [DNMT] inhibitor). In cells from both sources, DNA methylation at the NOS3 promoter was measured using methylation specific pyro sequencing, and endothelial gene expression was measured using RT PCR. Results: HC diet increased plasma cholesterol level from 75 mg/dl on CD to a plateau of about 540 mg/dl within 2 weeks. Endothelial NOS3 expression was significantly reduced (71±9 % of CD) after 4 weeks of HC, a level sustained at subsequent time points. Withdrawal of HC for 8 weeks did not recover NOS3 expression. After 12-week HC, the NOS3 promoter was hypermethylated. Withdrawal of HC did not reverse NOS3 promoter methylation. In vitro treatment of HAEC with human LDL (200 mg/dl total cholesterol) or GW3956 (5μM) suppressed NOS3 mRNA to 50% and 30% respectively, suggesting that LXR/RXR is involved in suppression of NOS3. Nitric oxide production was consistently suppressed by GW3959. Both could be reversed through inhibition of DNMTs by RG108. Conclusions: DNA methylation and LXR/RXR pathway can mediate the HC-suppression of endothelial NOS3. The study identifies novel pharmaceutical targets in treating endothelial dysfunction. Crosstalk between these pathways is under investigation.

scholarly journals Mangosteen Pericarp Inhibits Nuclear Factor ?B (NF-?B) Activation and Reduces Expression of ICAM-1 in High Cholesterol Diet Rat

2013 ◽  
pp. 23-32
Author(s):  
H Hendarto ◽  
Mohammad Saifur Rohman ◽  
Djanggan Sargowo
Keyword(s):  
Crude Extract ◽  
High Fat Diet ◽  
Inhibitory Effect ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Factor B ◽  
Underlying Risk Factor ◽  
Underlying Risk

Background: Atherosclerosis is widely viewed as an inflammatory disease with hypercholesterolemia being a dominant underlying risk factor. This study aimed to determine the effect of mangosteen pericarp in inhibition of NF-?B activation and ICAM-1 expression in rat fed with high cholesterol.Methods and Results: Various doses of crude extract mangosteen pericarp were administered to the high fat diet wistar rats and the activity of NF-?B measured by immunohistochemistry to assess nuclear NF-?B expression and the ICAM-1 expression. The high fat diet resulted significant increased serum LDL levels. Increased nuclear NF- ?B activation and ICAM-1 expression were also observed in high fat diet rats in concurrence with increased serum LDL. The inhibitory effect on NF- ?B activity and ICAM-1 expression was observed when 400 mg of mangosteen pericarp crude extract was administered and even showed a higher inhibitory effect in 800 mg of mangosteen pericap treated rats. The 800 mg extract treatment resulted in decreased ICAM-1 expression similar to those of non high fat rats.Conclusion: The administration of 800 mg mangosteen pericarp crude extract significantly inhibited NF-?B activation and reversed the expression of ICAM -1 to the normal level in high cholesterol diet rats.

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