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alpha fructose/necrosis
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14 resultados
Impact of exercise and angiotensin converting enzyme inhibition on tumor necrosis factor-alpha and leptin in fructose-fed hypertensive rats.
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The aim of this study was to evaluate the effects of moderate-intensity regular exercise and/or an angiotensin converting enzyme (ACE) inhibition on tumor necrosis factor-alpha (TNF-alpha) and glucose and lipid metabolism parameters. Spontaneously hypertensive rats (SHRs) were fed a fructose-rich
Soy protein prevents renal damage in a fructose-induced model of metabolic syndrome via inhibition of NF-kB in male rats.
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The study determines the effect of soy protein on inflammatory status and expression of nuclear factor-kappa B (NF-κB P(65)) and receptor for advanced glycation end products (RAGE) in a metabolic syndrome (MS) model. MS was induced in adult male rats by feeding them a high fructose diet (60 g/100 g
Musa acuminata (Del Monte banana) lectin is a fructose-binding lectin with cytokine-inducing activity.
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A homodimeric, fructose-binding lectin was isolated from Del Monte bananas by using a protocol that involved ion-exchange chromatography on DEAE-cellulose and SP-Sepharose, and gel filtration by fast protein liquid chromatography on Superdex 75. Not only fructose, but also glucose, mannose, rhamnose
Apocynin administration prevents the changes induced by a fructose-rich diet on rat liver metabolism and the antioxidant system.
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In the present study, we investigated the role of NADPH oxidase in F (fructose)-rich-diet-induced hepatic OS (oxidative stress) and metabolic changes, and their prevention by apocynin co-administration. Wistar rats were fed for 21 days on (i) a control diet, (ii) a control diet plus 10% F in the
Fructose protects murine hepatocytes from tumor necrosis factor-induced apoptosis by modulating JNK signaling.
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Fructose-induced hepatic ATP depletion prevents TNF-induced apoptosis, whereas it contrarily enhances CD95-induced hepatocyte apoptosis in vitro and in vivo. By contrast, transformed liver cells are not protected against TNF due to metabolic alterations, allowing selective tumor targeting. We
Intestinal inflammatory profile shows increase in a diversity of biomarkers in irritable bowel syndrome.
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Background: It has been proposed that irritable bowel syndrome (IBS) is a low-grade mucosal inflammatory disease.Objective: To characterize the intestinal inflammatory profile in IBS patients with or without fructose intolerance.Design: Patients referred to colonoscopy with IBS
Pepino polyphenolic extract improved oxidative, inflammatory and glycative stress in the sciatic nerves of diabetic mice.
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The effect of pepino polyphenolic extract (PPE) on diabetic neuropathy was examined. Using HPLC/ESI-MS-MS analysis, PPE was demonstrated to contain coumaroyl and caffeoyl derivatives among polyphenols. PPE at 0.5 or 1% was supplied to diabetic mice for 12 weeks. The PPE intake at two doses
Effects of the Chinese medicine Jiang-Tang-Ke-Li on insulin resistance in fructose-fed rats.
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The aim of this study was to determine the effect of Jiang-Tang-Ke-Li (JTKL), a Chinese medicine used to treat diabetes mellitus, on insulin resistance and hypertension in fructose-fed rats (FFR). Six-week-old male Sprague-Dawley rats were fed either normal rat chow (control) or a fructose-rich chow
Physical activity offsets the negative effects of a high-fructose diet.
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OBJECTIVE
This study aimed to determine the interaction between a high-fructose diet and PA levels on postprandial lipidemia and inflammation in normal-weight, recreationally active individuals.
METHODS
Twenty-two men and women (age, 21.2 ± 0.6 yr; body mass index, 22.5 ± 0.6 kg · m(-2)) consumed an
Selective protection of human liver tissue in TNF-targeting of cancers of the liver by transient depletion of adenosine triphosphate.
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BACKGROUND
Tumor necrosis factor alpha (TNF) is able to kill cancer cells via receptor-mediated cell death requiring adenosine triphosphate (ATP). Clinical usage of TNF so far is largely limited by its profound hepatotoxicity. Recently, it was found in the murine system that specific protection of
Resveratrol and fenofibrate ameliorate fructose-induced nonalcoholic steatohepatitis by modulation of genes expression.
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OBJECTIVE
To evaluate the effect of resveratrol, alone and in combination with fenofibrate, on fructose-induced metabolic genes abnormalities in rats.
METHODS
Giving a fructose-enriched diet (FED) to rats for 12 wk was used as a model for inducing hepatic dyslipidemia and insulin resistance. Adult
The cell specificity of gene expression in the response to heat stress in corals.
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Previous transcriptional studies in heat-stressed corals have shown that many genes are responsive to generalized heat stress whereas the expression patterns of specific gene networks after heat stress show strong correlations with variation in bleaching outcomes. However, where these specific genes
Mitochondrial injury in steatohepatitis.
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Rich diet and lack of exercise are causing a surge in obesity, insulin resistance and steatosis, which can evolve into steatohepatitis. Patients with non-alcoholic steatohepatitis have increased lipid peroxidation, increased tumour necrosis factor-alpha (TNF-alpha) and increased mitochondrial
Dietary fructose causes defective insulin signalling and ceramide accumulation in the liver that can be reversed by gut microbiota modulation.
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Objective: The link between metabolic derangement of the gut-2013liver-visceral white adipose tissue (v-WAT) axis and gut microbiota was investigated. Methods: Rats were fed a fructose-rich diet and treated with an antibiotic mix. Inflammation was measured in portal plasma, ileum, liver, and v-WAT,
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