Curcumin improves the metabolic syndrome in high-fructose-diet-fed rats: role of TNF-α, NF-κB, and oxidative stress

2017 ◽  
Vol 95 (2) ◽  
pp. 140-150 ◽  
Author(s):  
Mohamed Elsayed Kelany ◽  
Tahir M. Hakami ◽  
Adel H. Omar
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Uric Acid ◽  
Serum Levels ◽  
Model Assessment ◽  
Lipid Peroxidation Product ◽  
Oxidation Stress ◽  
High Fructose Diet ◽  
High Fructose ◽  
Tnf Α

This study aimed to investigate effects of curcumin on high fructose diet (HFD)-induced metabolic syndrome (MetS) in rats and the possible mechanisms involved. MetS was induced in male albino rats (n = 20), over 8 weeks, by 65% HFD. For 8-week experiment period, rats were assigned to 2 equal groups: curcumin-treated rats received curcumin (200 mg/kg, p.o, once daily) along with HFD, and untreated rats were fed with HFD only. We evaluated body mass (BM), systolic blood pressure (SBP), homeostasis model assessment of insulin resistance (HOMA-IR), and serum levels of glucose, insulin, leptin, total cholesterol (TC), triglycerides (TGs), uric acid, malondialdehyde (MDA; lipid peroxidation product), and tumor necrosis factor-α (TNF-α; inflammatory cytokine), and serum catalase (endogenous antioxidant) activity and immunohistochemical expression of nuclear factor κB (NF-κB; inflammation-related transcription factor) in hepatocytes. HFD produced increases in BM, SBP, HOMA-IR, and serum levels of glucose, insulin, leptin, TC, TGs, uric acid, MDA, and TNF-α, a decrease in catalase activity, and strong positive expression of NF-κB in hepatocytes. Curcumin, in presence of HFD, produced significant improvements in all glucose and fat metabolism parameters, and in oxidative stress and inflammation biomarkers. Curcumin may potentially be useful in the treatment of MetS through its ability to modulate oxidation stress status and inflammation cascades.

scholarly journals Investigation of the effect of coffee on body weight, serum glucose, uric acid and lipid profile levels in male albino Wistar rats feeding on high-fructose diet

2019 ◽  
Vol 35 (1) ◽  
Author(s):  
Teka Obsa Feyisa ◽  
Daniel Seifu Melka ◽  
Menakath Menon ◽  
Wajana Lako Labisso ◽  
Mezgebu Legesse Habte
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
Uric Acid ◽  
Lipid Profile ◽  
Wistar Rats ◽  
Serum Glucose ◽  
Control Group ◽  
Fasting Serum ◽  
High Fructose Diet ◽  
High Fructose

AbstractCoffee is one of the most commonly consumed beverages in the worldwide and is assumed to have protective effects against metabolic syndrome. The present study was aimed at investigating the effect of coffee on body weight, serum glucose, uric acid and lipid profile levels in male albino Wistar rats feeding on high fructose diet. A post-test experimental study was conducted on a total of 30 (9–10 weeks old) male albino Wistar rats. The rats were divided into 6 groups: group I (normal control)-fed on standard chow and plain tap water only; group II (fructose control)-fed on standard chow and 20% of fructose solution; group III–VI (treatment groups)-fed on standard chow, 20% of fructose solution and treated with 71, 142, 213 and 284 mg/kg body weight/day of coffee respectively for six weeks. At the end, body weight, serum glucose, uric acid and lipid profile levels were investigated. Data was entered and cleared by epi-data software version 3.1 and analyzed by one way ANOVA followed by Tukey post hoc multiple comparison tests using SPSS V. 23.00. Statistical significance was considered at p < 0.05. The results showed that body weight, fasting serum glucose and uric acid levels significantly lowered in rats treated with 213 (p = 0.047; 0.049; 0.026) and 284 (p = 0.035; 0.029; 0.010) mg/kg body weight/day of coffee compared to fructose control group. Fasting serum triglycide (TG) and low density lipoprotein (LDL-C) levels showed significant reduction in rats treated with 284 mg/kg body weight/day of coffee as compared to fructose control group (p = 0.031; 0.046) respectively. In conclusion, treating rats with coffee decreased body weight, fasting serum glucose, uric acid, TC, TG and LDL-C, and increased HDL-C in a dose dependent manner in rats feeding on high fructose diet, suggesting that coffee consumption may be helpful in ameliorating metabolic syndrome.

scholarly journals Regulatory landscape of AGE-RAGE-oxidative stress axis and its modulation by PPARγ activation in high fructose diet-induced metabolic syndrome

2017 ◽  
Vol 14 (1) ◽  
Author(s):  
Luca Cannizzaro ◽  
Giuseppe Rossoni ◽  
Federica Savi ◽  
Alessandra Altomare ◽  
Cristina Marinello ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Stress Axis ◽  
High Fructose Diet ◽  
High Fructose ◽  
Regulatory Landscape

scholarly journals Impact of Hydroxychloroquine on Fructose-induced Metabolic Syndrome in Rats: Promising Protective Effect

2020 ◽  
Vol 8 (A) ◽  
pp. 153-159
Author(s):  
Ahmed Shata ◽  
Mahmoud A. Naga ◽  
Basem H. Elsawy ◽  
Abdel-Moneim Hafez
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Profile ◽  
Adhesion Molecule ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Model Assessment ◽  
Group Iii ◽  
Group I ◽  
High Fructose ◽  
Tnf Α

BACKGROUND: Hydroxychloroquine (HCQ) is used in the treatment of malaria and rheumatoid arthritis for a long time. Its effects on inflammation and immune modulation were noted. AIM: This study aims to investigate the effects of HCQ in fructose-induced metabolic syndrome and to explore its possible mechanisms. METHODS AND MATERIALS: Sixty male Sprague-Dawley rats were divided into Group I (negative control), Group II fed on high-fructose diet, and Group III fed on high fructose and subdivided into Group III-a (HCQ 50 mg/kg), Group III-b (HCQ 100 mg/kg), Group III-c (HCQ 200 mg/kg), and Group III-d (metformin 100 mg/kg). Body weight, blood glucose, liver enzymes, and lipid profile were measured. Insulin level, homeostatic model assessment (HOMA), soluble-intercellular adhesion molecule, and vascular cell adhesion molecule were assayed. Tumor necrosis factor (TNF)-α, adipokines (leptin, resistin, and adiponectin), and histological examination of pancreas were assessed. RESULTS: HCQ induces good effects on lipid profile and improves significantly HOMA, endothelial stress markers, and adiponectin, and reduces leptin and TNF-α levels. In addition, significant improvement in structural changes was noted in pancreas with different doses of HCQ. CONCLUSION: Favorable effects of HCQ in fructose-induced metabolic syndrome are promising and can be used early in those at risk of diabetes.

scholarly journals P0964EFFECTS OF XANTHINE OXIDASE INHIBITORS AND DAPAGLIFLOZIN ON RENAL GLUCOSE AND URATE TRANSPORTERS IN METABOLIC SYNDROME

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Hwee-Yeong Ng ◽  
Chien-Te Lee ◽  
Foong-Fah Leung ◽  
Yuai-Ting Lee
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Uric Acid ◽  
Xanthine Oxidase ◽  
Resistance Index ◽  
High Fructose Diet ◽  
Insulin Resistance Index ◽  
Xanthine Oxidase Inhibitors ◽  
High Fructose ◽  
Uric Acid Transporters

Abstract Background and Aims Metabolic syndrome consists of several medical conditions that collectively predict the risk for cardiovascular disease. Hyperglycemia and hyperuricemia are the major disorders of metabolic syndrome. Kidney reabsorbs almost all filtrated glucose by active transport at normal concentrations of plasma glucose via members of the sodium glucose transport (SGLT) family. Besides, the kidney plays a pivotal role in handling uric acid homeostasis. Uric acid is mainly controlled by urate transporter (UAT), urate anion exchanger 1 (URAT1) and glucose transporter 9 (GLUT9). The aims of the study were to determine the alteration of renal glucose and uric acid transporters in animals with metabolic syndrome after treatment of xanthine oxidase inhibitors and SGLT2 inhibitor. Method Sprague-Dawley rats were fed with normal chow (Control) or high fructose diet (60%) for totally 6 months. For those animals fed with high fructose diet for 3 months, they were divided into 4 groups including high fructose diet without treatment (FR), treatment with allopurinol (150 mg/L in drinking water), with febuxostat (30 mg/L in drinking water) or with dapagliflozin (1mg/kg/day intraperitoneal injection). Blood, urine and blood pressure were collected and measured at the end of study. Gene and protein expression of renal glucose and uric acid transporters were determined by reverse transcriptase polymerase chain reaction. The changes of transporters were then confirmed by immunohistochemical staining. Results High-fructose diet induced higher levels of fasting glucose, insulin resistance index, uric acid, triglyceride and blood pressure in FR group (all p &lt;0.05 vs. control). Treatment of allopurinol, febuxostat and dapagliflozin reduced body weight significantly. Fasting glucose, insulin resistance index and hyperuricemia were improved in all drug treatment groups (all p &lt;0.05). In the kidney, high fructose diet significantly upregulated SGLT1, SGLT2 and GLUT2 but downregulated GLUT1 expression. Urate transporters, including GLUT9, UAT and URAT1 were also increased (p &lt;0.05). The improvement of insulin resistance by xanthine oxidase inhibitors was associated with suppression of renal SGLT1, SGLT2 and GLUT2 expression. Dapagliflozin alleviated hyperuricemia and induced uricosuria without affecting serum xanthine oxidase activity. Compared to FR, dapagliflozin significantly inhibited fructose-induced overexpression of GLUT9, UAT and URAT1 in the kidney. Conclusion Long term high fructose diet induced metabolic syndrome in rats. Treatment of xanthine oxidase inhibitors and dapagliflozin ameliorated components of metabolic syndrome. Both allopurinol and febuxostat improved insulin resistance in association with suppression of renal SGLT1, SGLT2 and GLUT2 expression. Although dapagliflozin and xanthine oxidase inhibitors reduced uric acid in different mechanisms, they shared a similar molecular changes in the kidney by downregulating GLUT9, UAT and URAT1 expression.

Study Upon the Serum Level of Uric Acid and the Metabolic Syndrome Components

2019 ◽  
Vol 70 (3) ◽  
pp. 1062-1066
Author(s):  
Maria Rada ◽  
Delia Berceanu-Vaduva ◽  
Milan Velimirovici ◽  
Simona Dragan ◽  
Daniel Duda-Seiman ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Uric Acid ◽  
Serum Level ◽  
Abdominal Obesity ◽  
Cardiometabolic Risk ◽  
Serum Levels ◽  
Mean Value ◽  
The Metabolic Syndrome ◽  
Direct Association ◽  
Metabolic Syndrome Components

The serum level of uric acid (UA) appears to be associated with a variety of cardiometabolic risk factors; however, direct association with the metabolic syndrome (MetS) remains controversial. The aim of this study is to investigate the association between serum levels of UA and the components that define MetS, differentiated by gender. 262 patients were enrolled (132 women and 130 men); mean value of the age: 58.7�16 year. Hyperuricemia was considered when the level of serum UA �7mg/dL in men, and � 6mg/dL in women; MetS was defined according to the IDF criteria. The prevalence of MetS in the studied group was 35.11% and the prevalence of hyperuricemia was 16.79%. Men with hyperuricemia had the highest prevalence of abdominal obesity (87.5% vs. 66.32%, p [0.001) and hypertriglyceridemia (65.62% vs. 45.91%, p [ 0.001) versus men with normal level of serum UA. Women with hyperuricemia also had a significantly higher incidence of abdominal obesity (75% vs. 57.51%, p [0.001), hypertriglyceridemia (58.33% vs. 38.33%, p [0.001), decreased HDL (50% vs. 33.33%, p [0.001) and hyperglycemia (66.66% versus 50%, p [0.001) compared to those with normal levels of serum UA. The majority of men with hyperuricemia have more than 4 of the MetS components. Hyperuricemia had a higher prevalence in patients with MetS, it may be considered as a causal factor of MetS. Elevated levels of serum uric acid were significantly more associated with the increasing number of MetS components. Early detection and treatment of hyperuricemia is essential for preventing the metabolic syndrome and its complications.

TA-65, A Telomerase Activator improves Cardiovascular Markers in Patients with Metabolic Syndrome

2018 ◽  
Vol 24 (17) ◽  
pp. 1905-1911 ◽  
Author(s):  
Maria Luz Fernandez ◽  
Minu Sara Thomas ◽  
Bruno S. Lemos ◽  
Diana M. DiMarco ◽  
Amanda Missimer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Plasma Lipids ◽  
Disease Risk ◽  
Glycosylated Hemoglobin ◽  
Cardiovascular Disease Risk ◽  
Hdl Cholesterol ◽  
Double Blind ◽  
Tnf Α ◽  
Luminex Technology

Background: Telomerase Activator 65 (TA-65), a compound extracted from Astragalus membranaceus has been used in Chinese traditional medicine for extending lifespan. Scarce information exists on the effects of TA-65 on parameters of metabolic syndrome (MetS). Methods: We recruited 40 patients with MetS to determine the effects of TA-65 on dyslipidemias, hypertension, and oxidative stress in this at-risk population. The study was a double-blind, randomized crossover design in which patients were allocated to consume either 16 mg daily of a TA-65 supplement or a placebo for 12 weeks. Following a 3-week washout, participants were allocated to the alternate treatment for an additional 12 weeks. Anthropometric and biological markers were measured at the end of each treatment. Plasma lipids, glucose, CReactive Protein (CRP), liver enzymes, and glycosylated hemoglobin were measured using a Cobas c-111. Inflammatory cytokines were measured by Luminex technology and markers of oxidative stress by the use of spectroscopy. Results: Compared to the placebo period, HDL cholesterol (HDL-C) was higher while body mass index, waist circumference, and the LDL/HDL ratio were lower (p < 0.05) during TA-65 treatment. In addition, plasma tumor necrosis factor-α (TNF-α) was lower during the TA-65 period (p< 0.05). Positive correlations were observed in changes between the placebo and the TA-65 periods in HDL-C and CRP (r = -0.511, p < 0.01), alanine aminotransferase (r = -0.61, p < 0.001) and TNF-α (r = -0.550, p < 0.001) suggesting that the favorable changes observed in HDL were associated with decreases in inflammation. Conclusion: TA-65 improved key markers of cardiovascular disease risk, which were also associated with reductions in inflammation.

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