Changes induced by a fructose-rich diet on hepatic metabolism and the antioxidant system

CENEXA, Facultad de Ciencias Médicas, La Plata, Argentina.
Life sciences (Impact Factor: 2.7). 06/2010; 86(25-26):965-71. DOI: 10.1016/j.lfs.2010.05.005
Source: PubMed


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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Available from: Guillermo Schinella, Jun 24, 2015
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    • "Similarly, Pasko and colleagues [29] reported increased CAT activity in the testes of fructose-fed rats (310 mg/kg, 5 weeks), which implies that CAT is necessary for decomposition of toxic H 2 O 2 . By contrast, Francini et al [7] reported decreased CAT activity along with unaltered GPx activity with a 10% fructose diet, which may facilitate oxidative stress in rat liver. These findings reveal that fructose can induce oxidative stress, but the CAT response can be divergent in tissues. "
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    ABSTRACT: From ancient times, Dǎngshēn (Codonopsis javanica) has been used in Chinese traditional medicine. In this study we investigated the anti-hyperinsulinemia and antioxidant properties of C. javanica root extracts in a rat model of insulin resistance (IR), induced by chronic fructose feeding. Twenty-four Sprague–Dawley rats were randomized into control, fructose-treated (10%, w/v), and fructose then C. javanica (Fru + Cod)-treated groups. After 8 weeks fructose feeding, increased fasting serum insulin levels (2.6 ± 0.45 μg/L) and insulin area under the curve confirmed the IR (p < 0.001). However, C. javanica treatment to fructose-fed rats significantly attenuated the hyperinsulinemia with correspondingly improved glucose tolerance. Weight gain in Fru + Cod group was comparably (p < 0.01) lower than in the fructose-fed group. Furthermore, IR-induced increased hepatic lipid peroxidation, as demonstrated by elevated malondialdehyde levels, were significantly (p < 0.001) alleviated by C. javanica treatment. These findings reveal that chronic fructose intake may facilitate IR and oxidative damage, which could be eradicated by improved antioxidant status. Accordingly, we found that C. javanica treatment significantly improved the antioxidant enzyme activities, including superoxide dismutase, glutathione peroxidase and glutathione reductase in the liver. These findings that fructose-induced hyperinsulinemia and associated oxidative stress could be attenuated by C. javanica root extracts.
    Journal of Food and Drug Analysis 09/2013; 21(4). DOI:10.1016/j.jfda.2013.08.001 · 0.62 Impact Factor
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    • "In addition, high fructose consumption progresses to dietary model of type 2 diabetes that is associated with obesity, IR, hyperglycemia, and dyslipidemia [2]. Intake of either fat or fructose diet has been shown to trigger the free radicals or reactive oxygen species (ROS) production, thus ruining the antioxidant and inflammatory systems [5] [6] [7]. Many traditional ethnicities in East Asia and around the world believe that functional foods (fermented) are rich in nutrients and used as alternative medicine. "
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    ABSTRACT: Lactobacillus plantarum K68 (isolated from fu-tsai) and fruit-vegetable ferment (FVF) have been tested for antidiabetic, anti-inflammatory, and antioxidant properties in a rat model of insulin resistance, induced by chronic high fat-fructose diet. Fifty rats were equally assigned into control (CON), high fat-fructose diet (HFFD), HFFD plus K68, HFFD plus FVF, and HFFD plus both K68 and FVF (MIX) groups. Respective groups were orally administered with K68 (1 × 10(9) CFU/0.5 mL) or FVF (180 mg/kg) or MIX for 8 weeks. We found that HFFD-induced increased bodyweights were prevented, and progressively increased fasting blood glucose and insulin levels were reversed (P < 0.01) by K68 and FVF treatments. Elevated glycated hemoglobin (HbA1c) and HOMA-IR values were controlled in supplemented groups. Furthermore, dyslipidemia, characterized by elevated total cholesterol (TC), triglyceride (TG), and low-density lipoproteins (LDLs) with HFFD, was significantly (P < 0.01) attenuated with MIX. Elevated pro-inflammatory cytokines, interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α), were controlled (P < 0.01) by K68, FVF, and MIX treatments. Moreover, decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities were substantially (P < 0.01) restored by all treatments. Experimental evidences demonstrate that K68 and FVF may be effective alternative medicine to prevent HFFD-induced hyperglycemia, hyperinsulinemia, and hyperlipidemia, possibly associated with anti-inflammatory and antioxidant efficacies.
    Evidence-based Complementary and Alternative Medicine 04/2013; 2013:943020. DOI:10.1155/2013/943020 · 1.88 Impact Factor
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    • "De nombreux marqueurs du stress oxydant sont présents chez l'animal soumis à un régime très enrichi en fructose. Nous avons déjà décrit les liens entre NOsynthase et fructose, qui constituent un des mécanismes clés des effets délétères du fructose, en particulier via l'élévation de l'uricémie [7]. L'administration chronique d'apocynin, un inhibiteur de la NAD(P)H oxydase corrige la dysfonction traîne ni hypertriglycéridémie, ni baisse de la vitamine E, ni excès de peroxydation lipidique (TBARS). "
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    ABSTRACT: Fructose is a sugar present in small amount in few natural foods as fruits and honey. Its consumption has massively increased, especially in the U.S., because of huge quantities of syrups containing high quantities of fructose as in High Fructose Corn Syrups (HFCS), in relation to its industrial production, since the 60s, from starches corn, which can bring more than 80 g/day fructose by the large consumption of soft drinks and many processed foods. In recent decades, temporal patterns in HFCS intake have shown a close parallel with the upsurge in obesity. Rising levels of HFCS consumption has been implicated in the huge parallel surge of visceral adiposity, insulin resistance, hypertension, hyperuricemia, mixed dyslipidemia, metabolic syndrome, type 2 diabetes. The effects of excessive fructose are well documented in animals. In humans, its sole responsibility is denied by some authors. Sucrose intake, dietary fat, portion size are both largely responsible for this epidemic also. However fructose intake in diabetic subjects or situations as other cardiometabolic disorders can be acceptable only in small quantity and in foods naturally containing fructose (fruits and honey). This caloric sweetener seems to be avoided in metabolic disorders.
    Médecine des Maladies Métaboliques 10/2010; 4(5):521-529. DOI:10.1016/S1957-2557(10)70117-6
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