scholarly journals High fat / high cholesterol diet does not provoke atherosclerosis in the ω3-and ω6-polyunsaturated fatty acid synthesis inactivated Δ6-fatty acid desaturase deficient mouse

2021 ◽  
pp. 101335
Author(s):  
Wilhelm Stoffel ◽  
Erika Binczek ◽  
Inga Schmidt-Soltau ◽  
Susanne Brodesser ◽  
Ina Wegner
Keyword(s):  
Fatty Acid ◽  
Polyunsaturated Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Fatty Acid Desaturase ◽  
Acid Synthesis ◽  
High Cholesterol Diet ◽  
Deficient Mouse ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat

The effect of cranberry consumption on lipid metabolism and inflammation in human apo A-I transgenic mice fed a high-fat and high-cholesterol diet

2020 ◽  
pp. 1-8
Author(s):  
Christian Caceres ◽  
Mi-Bo Kim ◽  
Minkyung Bae ◽  
Tho X. Pham ◽  
Yoojin Lee ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Soleus Muscle ◽  
Hdl Cholesterol ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Expression Of Genes ◽  
Hdl Metabolism

Abstract Lipid metabolism and inflammation contribute to CVD development. This study investigated whether the consumption of cranberries (CR; Vaccinium macrocarpon) can alter HDL metabolism and prevent inflammation in mice expressing human apo A-I transgene (hApoAITg), which have similar HDL profiles to those of humans. Male hApoAITg mice were fed a modified American Institute of Nutrition-93M high-fat/high-cholesterol diet (16 % fat, 0·25 % cholesterol, w/w; n 15) or the high-fat/high-cholesterol diet containing CR (5 % dried CR powder, w/w, n 16) for 8 weeks. There were no significant differences in body weight between the groups. Serum total cholesterol, non-HDL-cholesterol and TAG concentrations were significantly lower in the control than CR group with no significant differences in serum HDL-cholesterol and apoA-I. Mice fed CR showed significantly lower serum lecithin–cholesterol acyltransferase activity than the control. Liver weight and steatosis were not significantly different between the groups, but hepatic expression of genes involved in cholesterol metabolism was significantly lower in the CR group. In the epididymal white adipose tissue (eWAT), the CR group showed higher weights with decreased expression of genes for lipogenesis and fatty acid oxidation. The mRNA abundance of F4/80, a macrophage marker and the numbers of crown-like structures were less in the CR group. In the soleus muscle, the CR group also demonstrated higher expression of genes for fatty acid β-oxidation and mitochondrial biogenesis than those of the control. In conclusion, although CR consumption elicited minor effects on HDL metabolism, it prevented obesity-induced inflammation in eWAT with concomitant alterations in soleus muscle energy metabolism.

scholarly journals Maternal high fat diet induces impaired polyunsaturated fatty acid synthesis in adult female offspring in rats

2011 ◽  
Vol 70 (OCE4) ◽  
Author(s):  
S. P. Hoile ◽  
N. A. Irvine ◽  
C. Kelsall ◽  
C. Torrens ◽  
K. A. Lillycrop ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Polyunsaturated Fatty Acid ◽  
Adult Female ◽  
Fatty Acid Synthesis ◽  
High Fat Diet ◽  
Acid Synthesis ◽  
Female Offspring ◽  
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.

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