scholarly journals Effect of Pioglitazone, Simvastatin and Their Combination on Adiponectin and TNF‐α Level in the Metabolic Syndrome: Novel Findings from the High Fructose‐Fed Rat Model.

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Noha N Nassar ◽  
Mona F Schaalan
Keyword(s):  
Metabolic Syndrome ◽  
Rat Model ◽  
The Metabolic Syndrome ◽  
High Fructose ◽  
Tnf Α ◽  
Α Level

scholarly journals Improvement of Cardiac Fibrosis Biomarkers through Inflammation Inhibition by Green Tea and Decaffeinated Light Roasted Green Coffee Extract Combination Administration in Metabolic Syndrome Rat Model

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 1013
Author(s):  
Mifetika Lukitasari ◽  
Mohammad Saifur Rohman ◽  
Dwi Adi Nugroho ◽  
Nila Aisyah Wahyuni ◽  
Mukhamad Nur Kholis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Green Tea ◽  
Rat Model ◽  
Cardiac Fibrosis ◽  
Significant Risk ◽  
Green Coffee ◽  
The Metabolic Syndrome ◽  
Tnf Α ◽  
Tgf Β1

Background: Metabolic syndrome is a significant risk factor for cardiovascular diseases. Green tea and green coffee extracts, antioxidant and anti-inflammatory agents may participate in metabolic syndrome-induced cardiac fibrosis alleviation. However, the effect of combination of those extracts still needs exploration. Therefore, this study investigated the effect of green tea and decaffeinated light roasted green coffee extracts and their combination in metabolic syndrome-induced cardiac fibrosis rats. Methods: Metabolic syndrome rat model was i1nduced through high-fat high sucrose diets feeding for 8 weeks and injection of low dose streptozotocin at the 2nd week. The metabolic syndrome rats were divided into 4 experimental groups metabolic syndrome rats (MS); metabolic syndrome rats treated with 300 mg/ kg b.w green tea extract (GT); metabolic syndrome rats treated with 200 mg/ kg b.w decaffeinated light roasted green coffee extract (GC); metabolic syndrome rats treated with the combination of the two extracts (CE); and a normal control (NC) group was added. Angiotensin 2 level was analyzed by ELISA method. Gene expression of NF-κB, TNF-α, IL-6, Tgf-β1, Rac-1, and α-sma were analyzed by touchdown polymerase chain reaction methods. Results: Metabolic syndrome rats treated with green tea and decaffeinated light roasted green coffee significantly decreased angiotensin-2 serum level and cardiac inflammation and fibrosis gene expression level (NF-κB, TNF-α, IL-6, Tgf-β1, Rac-1, and α-sma). More significant alleviation was observed in the combination group. Conclusion: This study suggested that combination of green tea and decaffeinated light roasted green coffee extracts showed better improvement in metabolic syndrome-induced cardiac fibrosis rat model compared to that of single extract administration through inflammation inhibition

Effects of TNF-α antagonist infliximab on fructose-induced metabolic syndrome in rats

2020 ◽  
pp. 096032712096996
Author(s):  
Yasmine A Abdelhamid ◽  
Mohammed F Elyamany ◽  
Muhammad Y Al-Shorbagy ◽  
Osama A Badary
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
Adult Population ◽  
Health Issues ◽  
Serum Triglycerides ◽  
Fructose Intake ◽  
The Metabolic Syndrome ◽  
High Fructose ◽  
Affect Body Weight ◽  
Tnf Α

Public health issues have been raised regarding fructose toxicity and its serious metabolic disorders. Deleterious effects of high fructose intake on insulin sensitivity, body weight, lipid homeostasis have been identified. The new millennium has witnessed the emergence of a modern epidemic, the metabolic syndrome (MS), in approximately 25% of the world’s adult population. The current study aimed to investigate the effect of the TNF-α antagonist infliximab on fructose-induced MS in rats. Rats were administered fructose (10%) in drinking water for 12 weeks to induce the experimental MS model. infliximab (5 mg/kg) was injected once weekly intraperitoneally starting on the 13th week for 4 weeks. Increase in body weight, blood glucose level, serum triglycerides (TGs), adiponectin level and blood pressure were present in MS rats. They also prompted increases in serum of leptin, TNF-α, and malondialdehyde (MDA) levels. Treatment with infliximab did not affect body weight, hyperglycemia or hypertension, but decreased serum TGs and increased serum HDL-c levels. Infliximab also decreased adiponectin levels. Surprisingly, infliximab increased MDA above its value in the MS group. These results reflect the fact that infliximab affects the manifestations of MS in rats. Though infliximab reduced TGs, increased HDL-c levels, reversed adiponectin resistance occurred by fructose, the drug failed to combat MS-mediated hyperglycemia, hypertension, and elevated MDA above the insult.

scholarly journals Effect of PPAR-γ Agonist on Adiponectin Levels in the Metabolic Syndrome: Lessons From the High Fructose Fed Rat Model

2007 ◽  
Vol 20 (2) ◽  
pp. 206-210 ◽  
Author(s):  
Y SHARABI ◽  
M ORONHERMAN ◽  
Y KAMARI ◽  
I AVNI ◽  
E PELEG ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Rat Model ◽  
Ppar Γ ◽  
The Metabolic Syndrome ◽  
High Fructose

Habitual Physical Exercise Improves Macrophage IL-6 and TNF-α Deregulated Release in the Obese Zucker Rat Model of the Metabolic Syndrome

2011 ◽  
Vol 18 (2) ◽  
pp. 123-130 ◽  
Author(s):  
Leticia Martín-Cordero ◽  
Juan José García ◽  
María Dolores Hinchado ◽  
Elena Bote ◽  
Rafael Manso ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Physical Exercise ◽  
Rat Model ◽  
Zucker Rat ◽  
The Metabolic Syndrome ◽  
Obese Zucker Rat ◽  
Tnf Α

Abstract 1125: Mulberry Leaf Ameliorates The Production Of Adipocytokines By Inhibiting Oxidative Stress In White Adipose Tissue In db/db Mice

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Masayuki Sugimoto ◽  
Hidenori Arai ◽  
Yukinori Tamura ◽  
Toshinori Murayama ◽  
Koh Ono ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Metabolic Disorders ◽  
The Body ◽  
Mulberry Leaf ◽  
The Metabolic Syndrome ◽  
Pparγ Agonist ◽  
Tnf Α

Mulberry leaf (ML) is commonly used to feed silkworms. Previous study showed that ML ameliorates atherosclerosis. However, its mechanism is not completely understood. Because dysregulated production of adipocytokines is involved in the development of the metabolic syndrome and cardiovascular disease, we examined the effect of ML on the production of adipocytokines and metabolic disorders related to the metabolic syndrome, and compared its effect with that of a PPARγ agonist, pioglitazone (Pio). By treating obese diabetic db/db mice with ML, Pio, and their combination, we investigated the mechanism by which they improve metabolic disorders. In this study, db/+m (lean control) and db/db mice were fed a standard diet with or without 3% (w/w) ML and/or 0.01% (w/w) Pio for 12 weeks from 9 weeks of age. At the end of the experiment we found that ML decreased plasma glucose and triglyceride by 32% and 30%, respectively. Interestingly, administration of ML in addition to Pio showed additive effects; further 40% and 30% reduction in glucose and triglyceride compared with Pio treatment, respectively. Moreover, administration of ML in addition to Pio suppressed the body weight increase by Pio treatment and reduced visceral/subcutaneous fat ratio by 20% compared with control db/db mice. Importantly, ML treatment increased expression of adiponectin in white adipose tissue (WAT) by 40%, which was only found in db/db mice, not in control db/+m mice. Combination of ML and Pio increased plasma adiponectin concentrations by 25% and its expression in WAT by 17% compared with Pio alone. In contrast, ML decreased expression of TNF-α and MCP-1 by 25% and 20%, respectively, and the addition of Pio resulted in a further decrease of these cytokines by about 45%. To study the mechanism, we examined the role of oxidative stress. ML decreased the amount of lipid peroxides by 43% and the expression of NADPH oxidase subunits in WAT, which was consistent with the results of TNF-α and MCP-1. Thus our results indicate that ML ameliorates adipocytokine dysregulation by inhibiting oxidative stress in WAT of obese mice, and that ML may have a potential for the treatment of the metabolic syndrome as well as reducing adverse effects of Pio.

Anti-Inflammatory Effects of Exercise on Metabolic Syndrome Patients: A Systematic Review and Meta-Analysis

2020 ◽  
pp. 109980042095806 ◽  
Author(s):  
Heidar Alizaei Yousefabadi ◽  
Arghavan Niyazi ◽  
Sahar Alaee ◽  
Mehrdad Fathi ◽  
Gholam Rasul Mohammad Rahimi
Keyword(s):  
Metabolic Syndrome ◽  
Exercise Training ◽  
Inflammatory Markers ◽  
Meta Analysis ◽  
Serum Levels ◽  
Future Research ◽  
The Metabolic Syndrome ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Training Impact

Background: Increments in inflammatory indicators and low levels of physical activity are correlated to the expansion of the metabolic syndrome (MetS). Objective: The purpose of this study was to establish if exercise training ameliorates inflammatory status in MetS patients. Data sources: PubMed, CINAHL, and Medline, Google Scholar, and Scopus databases and reference lists of included studies were searched. Study selection: Twenty randomized controlled trials (RCTs) of exercise-training impact on inflammatory markers (tumor necrosis factor (TNF) α, C-reactive protein (CRP), interleukin (IL) 6, IL-8, IL-10, and IL-18) with concurrent control groups were included in this analysis. Results: Results demonstrated an overall significant decrease in serum levels of TNF-α (mean difference (MD): −1.21 pg/ml; 95% confidence interval (CI): −1.77, −0.66), CRP (MD: −0.52 mg/l; 95% CI: −0.79, −0.25), IL-8 (MD: −1.31 pg/ml; 95% CI: −2.57, −0.06), and a significant increase in IL-10 (MD: 0.48 pg/ml; 95% CI: 0.10, 0.86). But exercise training did not change the level of IL-6 (MD: −0.69 pg/ml; 95% CI: −1.53, 0.14) and IL-18 (MD: −53.01 pg/ml; 95% CI: −166.64, 60.62). Conclusion: Exercise training improves TNF-α, CRP, IL-8, and IL-10 levels in patients with MetS. For some variables, isolated aerobic exercise, and combined aerobic and resistance exercise appears to be optimal. Future research is needed to clarify the mechanisms underlying exercise training’s effect on this population’s inflammatory markers. More studies are required to confirm these findings.

The change of proinflammatory cytokine tumor necrosis factor α level in the use of meloxicam in rat model of osteoarthritis

2019 ◽  
Vol 30 (6) ◽  
Author(s):  
Junaidi Khotib ◽  
Naning Windi Utami ◽  
Maria Apriliani Gani ◽  
Chrismawan Ardianto
Keyword(s):  
Tumor Necrosis Factor ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Treatment Groups ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Osteoarthritis (OA) is a chronic disease in the joints. One of the proinflammatory cytokines that is thought to have a major role in the inflammatory process, the emergence of pain, and cartilage damage in OA is tumor necrosis factor α (TNF-α). Meloxicam is a nonsteroidal anti-inflammatory drug class of drugs that is relatively selective in inhibiting the activity of cyclooxygenase 2 (COX-2) formation. This study is conducted to prove the change in TNF-α level in the use of meloxicam with model in animals suffering from OA. Methods The OA rat model was induced with sodium monoiodoacetate intra-articularly. Rats were divided into 5 groups: negative control group, positive control group, and treatment groups with various doses of meloxicam. Hyperalgesia effect was evaluated using a warm plate test, and TNF-α level was determined using enzyme-linked immunosorbent assay. Results The treatment groups that received meloxicam at a dose of 1.0, 3.0, or 10.0 mg/kg body weight (BW) did not show significant differences in rat knee joint diameter (p = 0.99), but showed a significant difference in sensitivity to heat stimulation (p = 0.02) compared to the control group. Osteoarthritis rats experienced a significant reduction in TNF-α level after being given meloxicam at a dose of 10 mg/kg BW compared with the control group. This shows that the 10 mg/kg BW of meloxicam is a potential dose in reducing the TNF-α level in OA rat models. Conclusions Based on these data, it can be concluded that the inhibition of pain and the development of OA by meloxicam in animal models may be assigned to a decreased level of TNF-α.

METFORMIN ADMINISTRATION TO A RAT MODEL OF THE METABOLIC SYNDROME

2004 ◽  
Vol 22 (Suppl. 1) ◽  
pp. S110
Author(s):  
C BN Ferreira ◽  
M LR Cesaretti ◽  
M Ginoza ◽  
M T Zaneila ◽  
A B Ribeiro ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Rat Model ◽  
The Metabolic Syndrome
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