scholarly journals FXR activation promotes intestinal cholesterol excretion and attenuates hyperlipidemia in SR‐B1‐deficient mice fed a high‐fat and high‐cholesterol diet

2020 ◽  
Vol 8 (5) ◽  
Author(s):  
Amar B. Singh ◽  
Bin Dong ◽  
Fredric B. Kraemer ◽  
Jingwen Liu
Keyword(s):  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Cholesterol Excretion ◽  
Deficient Mice

scholarly journals Perilla Oil Supplementation Ameliorates High-Fat/High-Cholesterol Diet Induced Nonalcoholic Fatty Liver Disease in Rats via Enhanced Fecal Cholesterol and Bile Acid Excretion

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Ting Chen ◽  
Fahu Yuan ◽  
Hualin Wang ◽  
Yu Tian ◽  
Lei He ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver Disease ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Perilla Oil ◽  
Cholesterol Excretion ◽  
Fecal Cholesterol

Recent experimental studies and clinical trials have shown that hepatic cholesterol metabolic disorders are closely related to the development of nonalcoholic fatty liver disease (NAFLD). The main goal of this study was to investigate the efficacy of the perilla oil rich in alpha-linolenic acid (ALA) against NASH and gain a deep insight into its potential mechanisms. Rats were fed a high-fat/high-cholesterol diet (HFD) supplement with perilla oil (POH) for 16 weeks. Routine blood biochemical tests and histological staining illustrated that the perilla oil administration improved HFD-induced hyperlipidemia, reduced hepatic steatosis, and inhibited hepatic inflammatory infiltration and fibrosis. Perilla oil also increased fecal bile acid and cholesterol excretion. Hepatic RNA-Seq analysis found that the long time perilla oil supplement notably modified the gene expression involved in cholesterol metabolism. Our results implicate that, after long-term high level dietary cholesterol feeding, rat liver endogenous synthesis of cholesterol and cholesterol-rich low density lipoprotein uptake was significantly inhibited, and perilla oil did not modulate expression of genes responsible for cholesterol synthesis but did increase cholesterol removed from hepatocytes by conversion to bile acids and increased fecal cholesterol excretion.

scholarly journals Cholesterol 7α-hydroxylase-deficient mice are protected from high-fat/high-cholesterol diet-induced metabolic disorders

2016 ◽  
Vol 57 (7) ◽  
pp. 1144-1154 ◽  
Author(s):  
Jessica M. Ferrell ◽  
Shannon Boehme ◽  
Feng Li ◽  
John Y. L. Chiang
Keyword(s):  
Metabolic Disorders ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Deficient Mice

Regulation of direct transintestinal cholesterol excretion in mice

2008 ◽  
Vol 295 (1) ◽  
pp. G203-G208 ◽  
Author(s):  
Astrid E. van der Velde ◽  
Carlos L. J. Vrins ◽  
Karin van den Oever ◽  
Ingar Seemann ◽  
Ronald P. J. Oude Elferink ◽  
...  
Keyword(s):  
Bile Salt ◽  
High Fat Diet ◽  
Dietary Factors ◽  
The Body ◽  
Phospholipid Content ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Cholesterol Excretion

Biliary secretion is generally considered to be an obligate step in the pathway of excess cholesterol excretion from the body. We have recently shown that an alternative route exists. Direct transintestinal cholesterol efflux (TICE) contributes significantly to cholesterol removal in mice. Our aim was to investigate whether the activity of this novel pathway can be influenced by dietary factors. In addition, we studied the role of cholesterol acceptors at the luminal side of the enterocyte. Mice were fed a Western-type diet (0.25% wt/wt cholesterol; 16% wt/wt fat), a high-fat diet (no cholesterol; 24% wt/wt fat), or high-cholesterol diet (2% wt/wt), and TICE was measured by isolated intestinal perfusion. Bile salt-phospholipid mixtures served as cholesterol acceptor. Western-type and high-fat diet increased TICE by 50 and 100%, respectively. In contrast, the high-cholesterol diet did not influence TICE. Intestinal scavenger receptor class B type 1 (Sr-B1) mRNA and protein levels correlated with the rate of TICE. Unexpectedly, although confirming a role for Sr-B1, TICE was significantly increased in Sr-B1-deficient mice. Apart from the long-term effect of diets on TICE, acute effects by luminal cholesterol acceptors were also investigated. The phospholipid content of perfusate was the most important regulator of TICE; bile salt concentration or hydrophobicity of bile salts had little effect. In conclusion, TICE can be manipulated by dietary intervention. Specific dietary modifications might provide means to stimulate TICE and, thereby, to enhance total cholesterol turnover.

scholarly journals Aspirin Attenuates the Initiation but Not the Progression of Atherosclerosis in Apolipoprotein E-Deficient Mice Fed a High-Fat, High-Cholesterol Diet

2004 ◽  
Vol 95 (1) ◽  
pp. 15-19 ◽  
Author(s):  
Mònica Tous ◽  
Natàlia Ferré ◽  
Elisabet Vilella ◽  
Francesc Riu ◽  
Jordi Camps ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Deficient Mice ◽  
Progression Of Atherosclerosis

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.

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