scholarly journals The effect of a probiotic on faecal and liver lipid classes in rats

1995 ◽  
Vol 73 (5) ◽  
pp. 701-710 ◽  
Author(s):  
Michihiro Fukushima ◽  
Masuo Nakano
Keyword(s):  
Basal Diet ◽  
Experimental Period ◽  
Cholesterol Concentration ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Control Groups ◽  
Probiotic Group

The effect of a probiotic composed ofBacillus, Lactobacillus, Streptococcus, SaccharomycesandCandidaspecies (each at 107–8colony-forming units (cfu)/g rice bran), given at a level of 150 g/kg diet for 6 weeks, on lipid metabolism was examined in the faeces, serum and liver of male rats. Liver weight decreased 35% in the rats fed on a high-fat, high-cholesterol diet containing the probiotic. Total cholesterol concentration in the serum was significantly lower in the probiotic group than in the control group throughout the experimental period in rats fed on the high-fat, high-cholesterol diet, and HDL-cholesterol concentration was significantly higher (P< 0·05) in the probiotic group than in the control group which was fed for the 6 week experimental period on a basal diet. The serum VLDL + IDL + LDL cholesterol concentrations in the probiotic groups were reduced compared with those of the corresponding control groups. The probiotic groups fed on the high-fat, high-cholesterol diet and the basal diet had lower hepatic cholesterol concentrations than did the corresponding control groups (P< 0·05). Hydroxymethylglutaryl coenzyme A reductase (NADPH) (EC. 1.1.1.34) activity in the liver was lower in rats fed on the high-fat, high-cholesterol diet with the probiotic. The neutral and acidic steroid concentrations in faeces were higher in the probiotic group than in the control group fed on the high-fat, high-cholesterol diet.Escherichia colidecreased andBifidobacteriumandEubacteriumincreased in the faecal microflora of rats fed on the dietary probiotic.Lactobacillusin the probiotic groups was higher than that in the control groups. The present study shows that the probiotic promotesBifidobacteriumandEubacteriumin the faecal microflora, and reduces cholesterol levels in the serum and liver of rats.

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.

Impact of Long-term, High-fat, and High-cholesterol Diet on Murine Vertebrae Bones

2020 ◽  
Author(s):  
Frank Alexander Schildberg ◽  
Koroush Kabir ◽  
Jessica Bojko ◽  
Mona Khoury ◽  
Werner Masson ◽  
...  
Keyword(s):  
Bone Density ◽  
Genetic Factors ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Micro Ct ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
The Impact

AbstractAs the percentage of overweight individuals in the population rises, diseases associated with excess weight resulting from poor nutrition are becoming more and more widespread. So far, the influence of weight or nutrition on bone health has shown conflicting results. In the literature, the existing studies disagree about the effect of diet on bones. Therefore, this study investigated the impact of a long-term, high-fat, and high-cholesterol diet on the spine in a mouse model. Wild-type mice were randomly separated into two groups; one group received a high-fat and high-cholesterol diet, and a control group was fed with a regular diet since birth for a duration of 8 months. The first to fifth thoracic vertebrae were extracted and investigated using histology and micro-CT. Samples were analyzed regarding different parameters: percentage of bone structure compared to the whole vertebra and the amount and thickness of the trabeculae. Both methods of the analysis showed similar results. Diet did not have a significant impact on the bone density of the vertebrae. The micro-CT examination showed that the average bone percentage of the examined vertebra was 6% (p = 0.2330) higher in the control group compared to the diet group. The same tendency was demonstrated in histology even though with a smaller difference of only 5%. The results of both methods were comparable and showed trends for the influence of different diets but not significant impacts. In summary, this study showed that a high-fat and high-cholesterol diet has a slightly negative impact on bone density. In order to further analyze the effects of different diets on bone composition, structure, and density, additional long-term studies should be carried out, and more parameters such as movement and genetic factors should be analyzed. Furthermore, other parameters such as exercise and genetic factors that could have a secondary influence on obesity should be investigated.

Chronic intermittent hypoxia causes hepatitis in a mouse model of diet-induced fatty liver

2007 ◽  
Vol 293 (4) ◽  
pp. G871-G877 ◽  
Author(s):  
Vladimir Savransky ◽  
Shannon Bevans ◽  
Ashika Nanayakkara ◽  
Jianguo Li ◽  
Philip L. Smith ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Intermittent Hypoxia ◽  
Chronic Intermittent Hypoxia ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat

Obstructive sleep apnea (OSA) causes chronic intermittent hypoxia (CIH) during sleep. OSA is associated with nonalcoholic steatohepatitis (NASH) in obese individuals and may contribute to progression of nonalcoholic fatty liver disease from steatosis to NASH. The purpose of this study was to examine whether CIH induces inflammatory changes in the liver in mice with diet-induced hepatic steatosis. C57BL/6J mice ( n = 8) on a high-fat, high-cholesterol diet were exposed to CIH for 6 mo and were compared with mice on the same diet exposed to intermittent air (control; n = 8). CIH caused liver injury with an increase in serum ALT (461 ± 58 U/l vs. 103 ± 16 U/l in the control group; P < 0.01) and AST (637 ± 37 U/l vs. 175 ± 13 U/l in the control group; P < 0.001), whereas alkaline phosphatase and total bilirubin levels were unchanged. Histology revealed hepatic steatosis in both groups, with mild accentuation of fat staining in the zone 3 hepatocytes in mice exposed to CIH. Animals exposed to CIH exhibited lobular inflammation and fibrosis in the liver, which were not evident in control mice. CIH caused significant increases in lipid peroxidation in serum and liver tissue; significant increases in hepatic levels of myeloperoxidase and proinflammatory cytokines IL-1β, IL-6, and CXC chemokine MIP-2; a trend toward an increase in TNF-α; and an increase in α1(I)-collagen mRNA. We conclude that CIH induces lipid peroxidation and inflammation in the livers of mice on a high-fat, high-cholesterol diet.

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

Simvastatin Reduces Expression and Activity of Lipoprotein-Associated Phospholipase A2 in the Aorta of Hypercholesterolaemic Atherosclerotic Rabbits

2009 ◽  
Vol 37 (4) ◽  
pp. 1029-1037 ◽  
Author(s):  
Z Qiao ◽  
J Ren ◽  
H Chen
Keyword(s):  
Atherosclerotic Lesion ◽  
Statin Treatment ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Atherosclerotic Plaques ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Local Inflammatory Response ◽  
Plaque Instability ◽  
Significant Difference

Lipoprotein-associated phospholipase A2 (Lp-PLA2) contributes to atherosclerotic plaque instability and subsequent sudden coronary death. Statins are associated with decreased stroke risk and may improve stability of atherosclerotic plaques. The present study investigated the effect of simvastatin on expression of Lp-PLA2 levels in atherosclerotic plaques and on Lp-PLA2 activity in atherosclerotic aortas. Rabbits were a fed chow (control group) or a high-cholesterol diet (atherosclerosis group) for 12 weeks. An additional group on the high-cholesterol diet received simvastatin (5 mg/kg per day) for the last 4 weeks (simvastatin group). Lp-PLA2 activity in plasma and atherosclerotic aortas was significantly higher in the atherosclerosis group than in the control group and, consistent with this, abundant Lp-PLA2 protein was detected in plaques in the atherosclerosis group. Simvastatin significantly reduced Lp-PLA2 activity in plasma and aorta tissue, and reduced Lp-PLA2 protein level in atherosclerotic plaques. Whereas there was no significant difference in total atherosclerotic lesion area between simvastatin and atherosclerosis groups, simvastatin significantly reduced macrophage content, lipid retention and the intima/media ratio but increased the content of smooth muscle cells in atherosclerotic lesions. Thus, statin treatment markedly reduced Lp-PLA2 in both plasma and atherosclerotic plaques. This was associated with attenuation of the local inflammatory response and improved plaque stability.

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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