Low-Dose Aspirin Ameliorated Hyperlipidemia, Adhesion Molecule, and Chemokine Production Induced by High-Fat Diet in Sprague-Dawley Rats

2013 ◽  
Vol 75 (2) ◽  
pp. 97-106 ◽  
Author(s):  
Hui-Li Lin ◽  
Hsueh-Wei Yen ◽  
Su-Ling Hsieh ◽  
Li-Mei An ◽  
Kuo-Ping Shen
Cytokine ◽  
2020 ◽  
Vol 128 ◽  
pp. 154999 ◽  
Author(s):  
Thabsile J. Mahlangu ◽  
Phiwayinkosi V. Dludla ◽  
Vuyolwethu Mxinwa ◽  
Zibusiso Mkandla ◽  
Luca Tiano ◽  
...  

2018 ◽  
Vol 9 (5) ◽  
pp. 1033-1040 ◽  
Author(s):  
Lawrence J Coppey ◽  
Hanna Shevalye ◽  
Alexander Obrosov ◽  
Eric P Davidson ◽  
Mark A Yorek

2019 ◽  
Author(s):  
Tinashe Mutize ◽  
Phiwayinkosi V. Dludla ◽  
Zibusiso Mkandla ◽  
Bongani B. Nkambule

AbstractObjectiveTo assess peripheral lymphocyte DNA methylation profiles in prediabetes using a high fat-diet-fed C57BL/6 animal model. We further evaluated whether low dose-aspirin, or low-dose aspirin in combination with metformin, could modulate global DNA methylation levels in peripheral blood lymphocytes.MethodsTwenty-eight (28) male C57BL/6 mice were used in two experimental phases. The first experiment involved animals (n=16) which were randomised to receive a low-fat diet (LFD) or high-fat diet (HFD) (n = 8/group) for 10 weeks. Whereas in the second experiment, HFD-fed mice (n=15) were randomised into 3 treatment groups, a low-dose aspirin (LDA), LDA and metformin group, and a clopidogrel group. DNA methylation profiles of were determined using flow cytometry.ResultsThe HFD group showed moderate weight gain and elevated postprandial blood glucose levels when compared to the LFD group after 2 weeks of HFD-feeding (p < 0.05). Interestingly, the HFD group had elevated levels of T cells expressing high levels %5-methylcytosine (p<0, 05). Notably, these elevated levels were lowered by short-term low-dose aspirin treatment.DiscussionT cells are involved in the propagation of the inflammatory response. Persistent T cell activation promotes chronic inflammation and insulin resistance. Low-dose aspirin may be effective in modulating T cell-specific global methylation.


2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
M. S. Crawford ◽  
A. E. Mohr ◽  
K. L. Sweazea

Diet-induced obesity and metabolic syndrome are associated with the onset of gastrointestinal diseases, such as hepatic steatosis and gut inflammation. Prior research shows that a proprietary soil-derived organic mineral complex (OMC) prevents hyperglycemia, endotoxemia, and liver injury in rats fed a high-fat diet (HFD) for 10 weeks. The aim of this study was to further examine the effects of OMC on the liver and gastrointestinal health of these rats. Six-week-old male Sprague-Dawley rats (n = 36) were divided into two dietary groups: Chow or HFD fed for 10 weeks. Animals were further divided (n = 6/group) and administered 0, 0.6, or 3.0 mg/mL OMC in their drinking water. The 10-week HFD resulted in significant liver fat accumulation. Both OMC doses prevented hepatic increases in the glycation end product Nε-(carboxymethyl)lysine (CML) induced by HFD ( p < 0.05 ). Low-dose OMC was associated with higher expression of occludin in the small intestine of rats fed either diet (two-way ANOVA, p < 0.042 ). Linear discriminant analysis (LDA) effect size (LEfSe) indicated significant differences in fecal microbial composition of untreated HFD-fed rats in comparison to untreated Chow rats at 10 weeks (LDA score > 2.0 : 18). After 10 weeks, untreated HFD-fed rats were also more abundant in bacteria associated with obesity and metabolic disease in comparison to corresponding week 0 samples (LDA score > 2.0 : 31), 10-week untreated Chow (LDA > 2.0 : 18), or 10-week OMC-treated HFD-fed rats (0.6 mg/mL; LDA > 2.0 : 80, 3.0 mg/mL; LDA > 2.0 : 8). Low-dose OMC prevented the HFD-induced increase in the Firmicutes-to-Bacteroidetes (F/B) ratio ( p < 0.0416 ). Study animals treated with OMC exhibited no significant changes in the gut microbiota at week 10, although gut inflammatory biomarkers were not significantly altered by diet or OMC treatment. These results indicate that OMC supplementation ameliorates glycosylation reactions and modifies HFD-induced alterations in the intestinal microbiota.


2020 ◽  
Vol 7 ◽  
pp. 100047
Author(s):  
Kabelo Mokgalaboni ◽  
Phiwayinkosi V. Dludla ◽  
Zibusiso Mkandla ◽  
Tinashe Mutize ◽  
Tawanda Maurice Nyambuya ◽  
...  

Metabolism ◽  
2021 ◽  
Vol 116 ◽  
pp. 154497
Author(s):  
Elif Günalan ◽  
Meyli Ezgi Karagöz ◽  
Bayram Yılmaz ◽  
Burcu Gemici

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Michael J Duryee ◽  
Anand Dusad ◽  
Scott W Shurmur ◽  
Michael D Johnston ◽  
Robert P Garvin ◽  
...  

Introduction Malondialdehyde/Acetaldehyde (MAA) modified proteins have been suggested to play a role in the development/progression of atherosclerosis. Circulating antibodies directed against these proteins have recently been shown to be associated with the severity of the disease. More specifically, the isotype of the antibody to MAA correlated with either an acute MI (IgG) or stable plaque formation (IgA) formation. MAA is thought to form as a result of the oxidation of fat(s) and thus the concentration and antibody response should reflect the amount of fat in the diet. Objective The purpose of this study was to evaluate the antibody responses to MAA modified proteins following immunization and high fat western diet feeding in rats. Methods Male Sprague Dawley rats were immunized with MAA-modified protein weekly for 5 weeks and then assayed for antibodies to these proteins. Animals were then separated into the following groups: chow sham, chow MAA immunized, high fat sham, and high fat MAA immunized. The high fat animals were fed a Western diet with 2-thiouracil for 12 weeks, bled every 3 weeks, and serum assayed for the presence of circulating MAA antibodies. Results Prior to feeding with high fat diet, rats immunized with MAA-modified protein had a significant increase (P<0.001) in serum antibodies directed against these modified proteins compared to controls (N of 4 per group). Following feeding of high fat diet antibody concentrations increased 6 fold in the high fat MAA immunized group compared to the chow MAA immunized group (P<0.05). Antibodies in the high fat sham and chow sham had only minimal increases in antibodies to these proteins. Conclusions These data demonstrate that following immunization with MAA-modified proteins, circulating antibodies are produced that increase following consumption of a high fat Western diet. It suggests that MAA-modified proteins are produced at low levels following normal diet, producing antibodies which act as a normal clearance method for altered protein. When high fat consumption increases these antibody levels are increased in response to the oxidative stress. Implications Use of these antibodies as a biomarker in the future may help predict the onset or progression of atherosclerosis.


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