Changes induced by a fructose-rich diet on hepatic metabolism and the antioxidant system.
ABSTRACT The effect of a three-week fructose-rich diet (FRD) upon gene expression, protein and activity levels of liver antioxidant system and carbohydrate metabolism was studied.
Serum glucose (fasting and after a glucose load), triglyceride and insulin levels of normal male Wistar rats were measured. In liver, we measured gene/protein expression and enzyme activity of catalase (CAT), copper-zinc-superoxide dismutase (CuZnSOD) and glutathione peroxidase (GSHPx); reduced glutathione (GSH); protein carbonyl content; thiobarbituric acid reactive substances (TBARS) content and microsomal membrane susceptibility to lipid peroxidation; glucokinase (GK), glucose-6-phosphatase (G-6-Pase) and glucose-6-phosphate dehydrogenase (G-6-PDH) activity; and glycogen, pyruvate, lactate and triglyceride content.
Similar body weights and caloric intake were recorded in both groups. FRD rats had higher serum glucose, insulin and triglyceride levels, molar insulin:glucose ratio, HOMA-IR values and impaired glucose tolerance, whereas CAT, CuZnSOD and GSHPx relative gene expression levels were significantly lower. CAT and CuZnSOD protein expression, CAT activity and GSH content were also lower, while protein carbonyl content was higher. No differences were recorded in CuZnSOD, MnSOD and GSHPx activity, TBARS content and membrane susceptibility to lipid peroxidation. Glycogen, lactate and triglyceride content and GK, G-6-Pase and G-6-PDH activity were significantly higher in FRD rats.
In the presence of oxidative stress, the liver exhibits changes in the carbohydrate and lipid metabolic pathways that would decrease reactive oxygen species production and their deleterious effect, thus inducing little impact on specific antioxidant mechanisms. This knowledge could facilitate the design and implementation of strategies to prevent oxidative stress-induced liver damage.
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ABSTRACT: Intake of dietary high fructose (HF) exerts a number of adverse metabolic effects. The present study was to investigate whether Artemisia sphaerocephala Krasch seed polysaccharides (ASKP) alleviated hyperglycemia, hepatic steatosis and oxidative injury in mice fed HF water. After 8 weeks of the experiment, administration of ASKP at 400 and 800mg/kg bw significantly reduced the fasting serum glucose, insulin concentrations and the homeostasis model assessment of basal insulin resistance (HOMA-IR) of the mice fed 20% HF water. In the oral glucose tolerance test, the administration of ASKP at 400 and 800mg/kg bw had a reduced plasma glucose concentrations after 15min of glucose loading in HF-fed mice, indicating that ASKP improved glucose intolerance. ASKP also remarkably ameliorated the HF-induced elevation of liver lipid contents and oxidative injury in mice, and caused the reduction of liver lipid peroxidation and the elevation of hepatic antioxidant system. Histopathology of the liver by conventional H&E and Oil Red O staining confirmed the liver steatosis and oxidative injury induced by HF diet and the hepatoprotective effect of ASKP. This is the first report showing that ASKP can ameliorate the high fructose-induced hyperglycemia, hepatic steatosis and oxidative injury.International journal of biological macromolecules. 05/2014;
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ABSTRACT: High fructose intake is associated with adverse metabolic syndromes. This study was designed to investigate whether the polysaccharides derived from Zizyphus jujube cv. Shaanbeitanzao (ZSP) could alleviate high fructose-induced insulin resistance and dyslipidemia in mice. ZSP was identified by capillary zone electrophoresis as an acidic heteropolysaccharide with l-arabinose, d-galactose and d-galacturonic acid being the main component monosaccharides. Mice were provided with 20% high-fructose water and ZSP was administered intragastrically at doses of 0, 200 or 400 mg kg(-1) BW for 4 weeks. Fructose-treated mice showed hyperglycemia, hyperinsulinemia and dyslipidemia with impaired insulin sensitivity (p < 0.05). Administration of ZSP at a dose of 400 mg kg(-1) BW significantly reduced the serum levels of glucose, insulin, TC, TG, LDL-C, and VLDL-C (p < 0.01). ZSP also markedly improved the HDL-C level, homeostasis model assessment for insulin resistance (HOMA-IR) and β-cell function (HOMA-β), and decreased the atherogenic index (AI) of the mice exposed to high-fructose water. Histopathological test with H&E and oil red O staining confirmed liver steatosis induced by a high-fructose diet and the hepatoprotective effect of ZSP. These findings indicate that the jujube polysaccharides may ameliorate insulin resistance and dyslipidemia in fructose-treated mice.Food & Function 06/2014; · 2.69 Impact Factor
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ABSTRACT: Background Islet NADPH oxidase activity is modulated by glucose and other insulin secretagogues and it might be part of the regulatory mechanism of insulin secretion. We studied its modulatory role of islet NADPH oxidase upon β-cell function in rats with fructose-induced oxidative stress. Methods Normal rats were fed for 3 weeks with a standard diet, a fructose-rich diet or both diets plus apocynin. We measured plasma glucose, insulin, triacylglycerol and lipid peroxidation levels and the homeostasis model assessment-insulin resistance (HOMA-IR) and HOMA-β indexes, and performed an oral glucose tolerance test. β-cell volume density and the number of islets per mm2 were determined by immunomorphometric analysis of the pancreas. Insulin secretion, glucose metabolism, glucokinase and NADPH oxidase activities were studied in islets isolated from each experimental group. Results Fructose-fed rats had increased plasma triacylglycerol, insulin and lipid peroxidation levels associated to an insulin resistance state; the reactive higher secretion was unable to cope with the increased demand of insulin, leading to an impaired glucose tolerance. They also have a lower number of islets per area unit with a decreased β-cell volume density. All these alterations were prevented by blocking NADPH oxidase activity with apocynin. Conclusion Fructose-induced changes are partly mediated by modulation of NADPH oxidase activity. General significance The metabolic dysfunctions and enhanced oxidative stress measured in fructose-fed rats resemble those recorded in human prediabetes; thus, successful strategies employed in this model could be later used to prevent the progression of this state towards type 2 diabetes in human beings.Biochimica et Biophysica Acta (BBA) - General Subjects 01/2014; · 3.85 Impact Factor