Methanol Extract of Sorbus Commixta Cortex Prevents Vascular Inflammation in Rats with a High Fructose-Induced Metabolic Syndrome

2007 ◽  
Vol 35 (02) ◽  
pp. 265-277 ◽  
Author(s):  
Dae Gill Kang ◽  
Eun Jin Sohn ◽  
An Sook Lee ◽  
Jin Sook Kim ◽  
Dae Ho Lee ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Methanol Extract ◽  
Vascular Inflammation ◽  
Diet Group ◽  
Expression Level ◽  
Moderate Increase ◽  
Sprague Dawley ◽  
The Metabolic Syndrome ◽  
High Fructose ◽  
Endothelial Nitric Oxide

Feeding high fructose (Frc) to rats induces a moderate increase in blood pressure, which is associated with insulin resistance. The present study was designed to evaluate the effect of the methanol extract of Sorbus commixta cortex (MSC) on vascular inflammation in a rat model of the metabolic syndrome induced by a high Frc-diet. Male Sprague-Dawley rats were divided into 4 groups and treated for 7 weeks as follows: 1) control, 2) high Frc-diet group, 3) Frc/MSC1 group; high Frc-diet group treated with MSC (100 mg/kg/day), and 4) Frc/MSC2 group; high Frc-diet group treated with MSC (200 mg/kg/day). High Frc-induced decreases of the expression level of aortic endothelial nitric oxide synthase (ecNOS) while the production of cyclic GMP (cGMP) was restored by treatment with MSC. On the contrary, increases of the expression level of endothelin-1 (ET-1) in the aorta, the transcription factor, the cytokine related with vascular inflammation, and the adhesion molecules were suppressed by MSC treatment. Moreover, MSC treatment was shown to lessen the thickening noted in the aortic intima and media of the high Frc-diet group. Our findings suggest that MSC may have an anti-vascular inflammatory effect on rats with a high Frc-induced metabolic syndrome.

Fructose, but not dextrose, accelerates the progression of chronic kidney disease

2007 ◽  
Vol 293 (4) ◽  
pp. F1256-F1261 ◽  
Author(s):  
Michael S. Gersch ◽  
Wei Mu ◽  
Pietro Cirillo ◽  
Sirirat Reungjui ◽  
Li Zhang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Tissue Homogenate ◽  
Glomerular Sclerosis ◽  
Sprague Dawley ◽  
Tubular Atrophy ◽  
High Fructose Diet ◽  
The Metabolic Syndrome ◽  
High Fructose

The metabolic syndrome has recently been recognized as a risk factor for kidney disease, but the mechanisms mediating this risk remain unclear. High fructose consumption by animals produces a model of the metabolic syndrome with hypertension, hyperlipidemia, and insulin resistance. The present study was conducted to test the hypothesis that consumption of a high-fructose diet could accelerate the progression of chronic kidney disease. Three groups of 14 male Sprague-Dawley rats were pair fed a specialized diet containing 60% fructose (FRU) or 60% dextrose (DEX) or standard rat chow (CON). After the animals were fed their assigned diet for 6 wk, five-sixths nephrectomy was performed, and the assigned diet was continued for 11 wk. Proteinuria was significantly increased and creatinine clearance was decreased in the FRU group compared with the CON and DEX groups, and blood urea nitrogen was higher in the FRU group than in the CON and DEX groups. Kidneys from the FRU group were markedly larger than kidneys from the CON and DEX groups. Glomerular sclerosis, tubular atrophy, tubular dilatation, and cellular infiltration appeared markedly worse in kidneys from the FRU group than in kidneys from the DEX and CON groups. Monocyte chemoattractant protein-1 (MCP-1) was measured in renal tissue homogenate and found to be increased in the FRU group. In vitro studies were conducted to determine the mechanism for increased renal MCP-1, and fructose stimulation of proximal tubular cells resulted in production of MCP-1. In conclusion, consumption of a high-fructose diet greatly accelerates progression of chronic kidney disease in the rat remnant kidney model.

scholarly journals Relevance of a Hypersaline Sodium-Rich Naturally Sparkling Mineral Water to the Protection against Metabolic Syndrome Induction in Fructose-Fed Sprague-Dawley Rats: A Biochemical, Metabolic, and Redox Approach

2014 ◽  
Vol 2014 ◽  
pp. 1-17 ◽  
Author(s):  
Cidália Dionísio Pereira ◽  
Milton Severo ◽  
João Ricardo Araújo ◽  
João Tiago Guimarães ◽  
Diogo Pestana ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Mineral Water ◽  
Tap Water ◽  
Magnesium Content ◽  
Atherosclerotic Cardiovascular Disease ◽  
Sprague Dawley ◽  
The Metabolic Syndrome ◽  
Sprague Dawley Rats ◽  
Calcium And Magnesium

The Metabolic Syndrome increases the risk for atherosclerotic cardiovascular disease and type 2 Diabetes Mellitus. Increased fructose consumption and/or mineral deficiency have been associated with Metabolic Syndrome development. This study aimed to investigate the effects of 8 weeks consumption of a hypersaline sodium-rich naturally sparkling mineral water on 10% fructose-fed Sprague-Dawley rats (Metabolic Syndrome animal model). The ingestion of the mineral water (rich in sodium bicarbonate and with higher potassium, calcium, and magnesium content than the tap water used as control) reduced/prevented not only the fructose-induced increase of heart rate, plasma triacylglycerols, insulin and leptin levels, hepatic catalase activity, and organ weight to body weight ratios (for liver and both kidneys) but also the decrease of hepatic glutathione peroxidase activity and oxidized glutathione content. This mineral-rich water seems to have potential to prevent Metabolic Syndrome induction by fructose. We hypothesize that its regular intake in the context of modern diets, which have a general acidic character interfering with mineral homeostasis and are poor in micronutrients, namely potassium, calcium, and magnesium, could add surplus value and attenuate imbalances, thus contributing to metabolic and redox health and, consequently, decreasing the risk for atherosclerotic cardiovascular disease.

scholarly journals Evalution of the castrated male Sprague–Dawley rat as a model of the metabolic syndrome and type 2 diabetes

2006 ◽  
Vol 30 (8) ◽  
pp. 1288-1297 ◽  
Author(s):  
B Christoffersen ◽  
K Raun ◽  
O Svendsen ◽  
C Fledelius ◽  
V Golozoubova
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Sprague Dawley ◽  
The Metabolic Syndrome ◽  
Sprague Dawley Rat

scholarly journals Amelioration of High Fructose Diet-Induced Insulin Resistance, Hyperuricemia, and Liver Oxidative Stress by Combined Use of Selective Agonists of PPAR-α and PPAR-γ in Rats

2020 ◽  
Vol 3 (2) ◽  
pp. 76-86
Author(s):  
Mahmoud M. Farag ◽  
Ehab H. Ashour ◽  
Wessam F. El-Hadidy
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Serum Insulin ◽  
Combined Treatment ◽  
Vehicle Group ◽  
Control Group ◽  
Peroxisome Proliferator ◽  
Ppar Γ ◽  
The Metabolic Syndrome ◽  
High Fructose

Background: The use of high-fructose (Fr) corn sweeteners and sucrose in manufactured food has markedly increased recently. This excessive Fr intake has been proposed in the etiology of the metabolic syndrome, which shows an increasing prevalence throughout the world. Objective: In this study, we questioned whether fenofibrate (FF), a peroxisome proliferator-activated receptor (PPAR)-α agonist, and pioglitazone (PG), a PPAR-γ agonist, might be effective in ameliorating the metabolic syndrome in a rat model. Materials and Methods: The metabolic syndrome was induced by feeding rats a high-Fr (60%) diet for 10 weeks. The rats were divided into 5 groups: control group, fed a normal rat chow; Fr + vehicle group; Fr + FF group; Fr + PG group; and Fr + (FF + PG) group (treated with both drugs). Drug or vehicle treatment was given daily for 6 weeks (from weeks 5 to 10). Thereafter, blood and liver samples were obtained for biochemical studies. Results: Rats fed a high-Fr diet developed hyperglycemia, hyperinsulinemia, hyperuricemia, hypertriglyceri­demia, and hypercholesterolemia, and had increased serum alanine aminotransferase, hepatic tumor necrosis factor-α, and malondialdehyde levels but decreases in both glutathione content and superoxide dismutase activity. Rat treatment with FF and/or PG attenuated these alterations. The improvement was greater with the combined treatment than with either drug alone, and normalization of insulin sensitivity was observed only in rats treated with the combination therapy. Conclusion: Acting on the 2 main PPAR subfamilies, the combination of FF and PG provides a more efficacious therapy for modulating the changes in serum insulin, uric acid, and lipids, as well as the accompanying hepatic inflammation and oxidative stress that characterize the Fr-induced metabolic syndrome.

scholarly journals Gastrodia elataAmeliorates High-Fructose Diet-Induced Lipid Metabolism and Endothelial Dysfunction

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Min Chul Kho ◽  
Yun Jung Lee ◽  
Jeong Dan Cha ◽  
Kyung Min Choi ◽  
Dae Gill Kang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Endothelial Dysfunction ◽  
Glucose Tolerance ◽  
Ethanol Extract ◽  
Oral Glucose ◽  
Gastrodia Elata ◽  
High Fructose ◽  
Amp Activated Protein Kinase ◽  
Endothelial Nitric Oxide

Overconsumption of fructose results in dyslipidemia, hypertension, and impaired glucose tolerance, which have documented correlation with metabolic syndrome.Gastrodia elata, a widely used traditional herbal medicine, was reported with anti-inflammatory and antidiabetes activities. Thus, this study examined whether ethanol extract ofGastrodia elataBlume (EGB) attenuate lipid metabolism and endothelial dysfunction in a high-fructose (HF) diet animal model. Rats were fed the 65% HF diet with/without EGB 100 mg/kg/day for 8 weeks. Treatment with EGB significantly suppressed the increments of epididymal fat weight, blood pressure, plasma triglyceride, total cholesterol levels, and oral glucose tolerance, respectively. In addition, EGB markedly prevented increase of adipocyte size and hepatic accumulation of triglycerides. EGB ameliorated endothelial dysfunction by downregulation of endothelin-1 (ET-1) and adhesion molecules in the aorta. Moreover, EGB significantly recovered the impairment of vasorelaxation to acetylcholine and levels of endothelial nitric oxide synthase (eNOS) expression and induced markedly upregulation of phosphorylation AMP-activated protein kinase (AMPK)αin the liver, muscle, and fat. These results indicate that EGB ameliorates dyslipidemia, hypertension, and insulin resistance as well as impaired vascular endothelial function in HF diet rats. Taken together, EGB may be a beneficial therapeutic approach for metabolic syndrome.

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