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Centre de Recherche en Nutrition Humaine d’Auvergne, Unité des Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 Saint-Genès-Champanelle, France
1To whom correspondence should be addressed. E-mail: yves.rayssiguier{at}clermont.inra.fr.
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ABSTRACT |
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 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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50%) in the OFS-supplemented fructose group compared with the other three groups. Fructose feeding in rats also significantly increased plasma (P < 0.001) and liver (P < 0.001) triglyceride (TG) concentrations and the addition of OFS prevented the TG accumulation induced by fructose in the liver (P < 0.05) and hyperlipemia (P < 0.05). OFS consumption prevented (P < 0.05) the lower plasma vitamin E/TG ratio in rats fed the fructose diet. Control rats fed the fructose diet had high plasma TBARS values compared with rats fed the starch diet, whereas TBARS values remained unchanged when rats were supplemented with OFS. Control rats fed the fructose diet had higher TBARS urine values and higher heart tissue susceptibility to peroxidation compared with rats fed the starch diet, and this effect was significantly reduced by OFS consumption. Further studies are required to identify the mechanisms underlying the protective effect of OFS against the pro-oxidant effect of fructose. However, the potential nutritional benefits of OFS supplementation in fructose-rich diets are suggested.
KEY WORDS: • high fructose diet • insulin • leptin • oligofructose • oxidative stress
Fructose intake has increased steadily during the past two decades (1). Although there is little evidence that modest amounts of fructose have detrimental effects on carbohydrate and lipid metabolisms, larger doses of fructose have been associated with numerous metabolic abnormalities in humans and laboratory animals (2,3). High sucrose and high fructose diets have been used in animal models to induce the metabolic changes designated syndrome X, a disorder in which insulin resistance, hypertension, dyslipidemia and high incidence of cardiovascular diseases were described (4,5). The underlying mechanisms for the detrimental consequences of a high fructose diet in animal models are not clear. However, the possibility that dietary fructose facilitates oxidative damage (6) is supported by recent data from our laboratory (7,8). An insulin sensitizer, metformin, has been shown to improve the free-radical defense system potential and insulin sensitivity (9), improve lipid metabolism and attenuate lipid peroxidation (10) in rats fed a high fructose diet. Dietary intervention aiming to ameliorate lipid disturbance and insulin sensitivity also includes supplementation with dietary fibers (11). Nondigestible oligosaccharides are a new category of low energy sweeteners that share many properties with fermentable dietary fibers. Short-chain oligofructose (OFS), which belongs to this class of food ingredients, resists hydrolysis by digestive enzymes, but is highly fermented in the cecum and the colon, producing SCFA (12). Previous work established that OFS decreased plasma lipids in rats (13). Given the pro-oxidant effect in rats fed a high fructose diet, the modification of the impact of fructose on oxidative stress, together with the hypolipemic effect by supplementation of a high fructose diet with OFS, was assessed.
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MATERIALS AND METHODS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Weaning male Wistar-Han rats (IFFA-CREDO; L’Arbresle, France), 6 wk old, weighing 
150 g were housed in wired-bottomed cages in a temperature-controlled room (22°C) with a 12-h light/12-h dark cycle. The rats were maintained and handled according to the recommendations of the INRA Ethics Committee, in accordance with decree no. 87-848. All rats were first adapted to a starch-based semipurified diet for 7 d. They were then randomly divided into four groups according to dietary carbohydrate and OFS supplementation as follows: starch (S), fructose, starch + OFS (S/OFS) and fructose + OFS (F/OFS) groups (10 per group), and fed their appropriate diets for 4 wk. Rats had unrestricted access to food and distilled water. The synthetic diets contained (in g/kg): casein, 200; starch or fructose, 650; corn oil, 50; alphacel, 50; DL-methionine, 3; choline bitartrate, 2; AIN-76 mineral mix, 35; AIN-76A vitamin mix, 10 (ICN Biomedicals, Orsay, France) (14). OFS-fed rats were fed diets containing (10 g/100 g) Raftilose P95 by replacing 10 g of carbohydrate, either starch or fructose, by 10 g of OFS. To reduce the diarrhea that may occur at the onset of administration of high doses of fermentable carbohydrates, OFS was administrated at the dose of 5 g/100 g during the first 4 d of the experiment and then at the dose of 10 g/100 g.
Chemicals.
Raftilose P95, a mixture of glucosyl-(fructosyl)n-fructose (64%) and (fructosyl)m-fructose (36%) with a mean degree of polymerization of 4.8, was used as the oligofructose source and was a gift from ORAFTI (Thienen, Belgium).
Sample collections.
At 4 d before sampling, rats were individually kept in stainless steel metabolic cages with unrestricted access to water and food. Urine samples were collected for 24 h at the end of the experiment in 50-mL graduated tubes attached to urine-collection funnels with a screen to prevent contamination from feces. Urine volumes were accurately measured and the samples were centrifuged and stored at -80°C until analysis. At the time of sampling (0900 h), rats were weighed, anesthetized with sodium pentobarbital (40 mg/kg body weight, intraperitoneally) and killed. Blood was collected from the abdominal aorta into heparinized tubes. Plasma obtained after low speed centrifugation (2000 x g, 15 min) was stored at -80°C for biochemical analysis. The heart and liver were rapidly removed, the liver was weighed and both organs were washed in ice-cold saline solution (9 g NaCl/L), then placed in liquid N2 and stored at -80°C before analysis. Cecum and cecal contents were sampled and weighed, and the pH of cecal contents was determined.
Analytical procedure.
SCFA were determined by GLC of portions of supernatant fractions of cecal contents using acetate (100 mmol/L), propionate (50 mmol/L) and butyrate (50 mmol/L) (Sigma, St. Louis, MO) as standards (15). Triglycerides (Biotrol, Paris, France) were determined in plasma by enzymatic procedures. Liver samples were homogenized and lipids were extracted with chloroform/methanol (2:1, v/v). Triglycerides in the lipid residue were saponified by 0.5 mol/L KOH-ethanol at 70°C for 30 min, then 0.15 mol/L MgSO4 was added to neutralize the mixture. After centrifugation (2000 x g, 5 min), the supernatant was assayed for glycerol (Biotrol). A polyvalent control serum (Biotrol-33-plus) was treated in parallel to samples and served to control the accuracy of the results in plasma and tissue lipid analysis.
Concentrations of plasma TBARS were determined by spectrofluorometry (LS 5; Perkin Elmer Cetus, Norwalk, CT). A modified method of Ohkawa et al. (16) was used as previously described (17).
TBARS concentrations in urine samples were measured as previously described (18) and calculated on the basis of 24-h urine volume. Plasma vitamin E was extracted twice with hexane and quantified by reversed-phase HPLC (HPLC apparatus, Kontron series 400; Kontron Instruments, St Quentin en Yvelines, France) as previously described (19). The column was a C18 (nucleosil; 250 mm long, I.D. 46 mm, 5-µm particles) purchased from Interchim (Montluçon, France). The sample loop size was 80 µL. The compounds were detected by UV (292 nm) then quantified by internal and external calibration by use of standard solutions of 
-tocopherol acetate and -tocopherol (Sigma). Copper concentrations in the liver were determined by a method combining dry heat and acid digestion (20). Samples were analyzed by flame atomic absorption at 324.7 nm by use of a Perkin–Elmer 800 atomic absorption spectrometer (Perkin Elmer) (21). Liver tissue was dry-ashed at 500°C for 12 h, and the ash was dissolved in nitric acid before analysis of copper content. National Institute of Standard and Technology Reference material (Office of Standard Reference, Gaithersburg, MD) was digested and analyzed along with samples to verify the accuracy. For the lipid peroxidation study of heart tissue, homogenates were prepared on ice by use of a ratio of 1 g wet tissue to 9 mL 150 mmol/L KCl using a Polytron homogenizer. By use of a spectrophotometer (Uvikon 941 plus series; Kontron Instruments), TBARS concentrations were measured in tissue homogenates after lipid peroxidation induced by FeSO4 (2 µmol/L)-ascorbate (50 µmol/L) for 30 min in a 37°C water bath in an oxygen-free medium, using a standard of 1,1,3,3-tetraethoxypropane, as previously described (17).
Plasma glucose concentrations were measured colorimetrically, according to Bergmeyer et al. (22), by the same method as for plasma glucose, after incubation with glucose oxydase. Plasma insulin concentrations were measured by homologous RIA using rat insulin standard (Linco Research, St. Charles, MO), in which the assay was 100% cross-reactive with rat and human insulin. The lowest limit of detection was 0.1 µg/L, and intra- and interassay variations were 2.7 and 3.1%, respectively. RIA of plasma leptin concentration used a homologous assay incorporating anti-rat leptin antibody and rat leptin as standard (Linco Research). The lowest limit of sensibility was 0.5 µg/L, and the intra- and interassay variations were 1.5 and 2.5%, respectively.
Statistical analysis.
Statistical analyses were performed using the Statview program (Abacus Concepts, Berkeley, CA). Data are expressed as means ± SEM. Data were analyzed by two-way ANOVA with carbohydrate and OFS the main effects tested. For significant F ratios, Fisher’s protected least-significant difference was used as a post hoc test on individual means. Differences were considered significant at P < 0.05.
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RESULTS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Fructose in the diet did not affect food intake and body weight. Body weight tended to be lower when OFS was added to the diet (P = 0.056). Regardless of the type of carbohydrate, OFS in the diet elicited an enlargement of the cecum in rats, largely corresponding to an accumulation of digesta in the cecum (+330%) and to hypertrophy of the cecal wall itself. Rats fed OFS-supplemented diets had a significantly higher SCFA cecum pool, which was greater in rats fed the fructose-rich diet supplemented with OFS than in rats fed the starch-based diet supplemented with OFS. Additionally, there were qualitative changes in the SCFA molar ratio. Although OFS supplementation resulted in a higher percentage of propionate regardless of type of carbohydrate, the percentage of butyrate was strongly elevated in rats fed the OFS-supplemented fructose diet (up to 25% of total SCFA instead of 12% in rats fed the starch diet supplemented with OFS) (Fig. 1). The cecal enlargement was associated with a significant acidification of the cecal contents of rats in the OFS-supplemented groups. However, the pH of cecal contents of the F/OFS group was slightly but significantly higher than that of the S/OFS group (P < 0.05).
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Fructose feeding in rats led to hypertriglyceridemia. Addition of OFS to the diet lowered the plasma TG concentrations in fructose-fed rats, but not in rats fed the starch diet. Plasma glucose concentrations among rats in the various dietary groups did not differ. Fructose feeding increased plasma fructose concentrations and the increase was significantly reduced in rats supplemented with OFS. Plasma insulin concentrations were higher (+63%) in the fructose-fed group than in the starch-fed group, whereas plasma insulin concentrations did not differ between the two groups supplemented with OFS. However, OFS tended (P < 0.10) to lessen the hyperinsulinemic effect of fructose. Plasma leptin concentrations did not differ according to the nature of the carbohydrate; however, the plasma leptin concentration was significantly lower (50%) in the OFS-supplemented fructose group than in the other three groups.
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Liver weight was significantly higher in fructose-fed rats than in starch-fed rats (P < 0.001) and was not affected by OFS supplementation. The increase in the liver TG concentrations induced by fructose feeding (P < 0.001) was prevented by OFS supplementation (P < 0.05). Fructose-fed rats also had lower liver copper concentrations compared with rats fed the starch-based diet. Furthermore, the liver copper concentrations were significantly higher in the F/OFS group than in the S/OFS group (P < 0.05).
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The hypolipemic effect in rats fed OFS-supplemented diets was accompanied by significantly lower plasma vitamin E concentrations, and the hyperlipemic effect of fructose was accompanied by a significantly lower vitamin E/TG ratio. The OFS consumption prevented (P < 0.05) the lower vitamin E/TG ratio in rats fed the fructose diet (carbohydrate and OFS interaction, P = 0.06). Rats fed the fructose diet had high plasma TBARS values compared with rats fed the starch diet. The TBARS values remained unchanged after OFS supplementation. The TBARS urine values were higher in rats fed the fructose diet than in rats fed the starch diet, and this effect was significantly reduced by OFS consumption. After exposure of heart homogenate to iron-induced lipid peroxidation, TBARS were significantly higher in rats fed the fructose diet, although TBARS values did not differ in rats supplemented with OFS.
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DISCUSSION |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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In agreement with previous studies (13,27), feeding rats a diet supplemented with OFS lowered TG plasma concentrations and prevented TG accumulation induced by fructose in the liver. This effect appears to be more important when fructose is the source of dietary carbohydrate, given that the TG-lowering effect in starch-fed rats compared with fructose-fed rats is, respectively, 20 and 28% in the liver and 16 and 33% in the plasma. The mechanism of the lowering effect of OFS on serum lipids remains incompletely elucidated. However, when OFS is added to a carbohydrate-rich diet, the TG-lowering action of OFS has been related mainly to a reduction of the de novo liver fatty acid synthesis (28,29). Additional studies should be of interest to determine whether the reduction in plasma TG could be explained by a reduction in the amount of VLDL particles or a reduction in the amount of TG in the VLDL particles. Dietary OFS also modifies the kinetic absorption of dietary carbohydrate, leading to modifications in lipid and glucose concentrations (30). Thus, lower glucose and insulin concentrations may contribute to the reduction in hepatic fatty acid and TG synthesis and thus to the hypolipidemic effect of OFS. Like other fermentable dietary fibers, OFS escapes digestion of the intestine and is fermented in the cecum, producing SCFA, mainly acetate, propionate and butyrate, which are efficiently absorbed (31). Butyrate serves as fuel for the mucosa, whereas acetate and propionate enter the portal blood and may influence systemic carbohydrate and lipid metabolisms (32). Because acetate and propionate have dissimilar effects on lipid metabolism (29), the pattern of OFS-induced fermentation might be important. The results clearly indicate that the pattern of carbohydrate fermentation is different in rats fed the starch-based diet from that in rats fed the fructose diet. The higher SCFA pool in rats fed the fructose diet than in rats fed the starch diet may result from the presence of more substrate. Thus it remains possible that OFS supplementation affects fructose absorption. The presence of fructose and nondigestible carbohydrate might result in increased osmotic pressure in the intestine. This hypothetical mechanism remains to be investigated.
The present experiment agrees with previous studies showing that the consumption of a high fructose diet has a pro-oxidant effect in rats. Previous studies showed that the consumption of a high fructose diet negatively affects the balance between free radical production and antioxidant defense in rats, leading to increased lipid susceptibility to peroxidation (7,8). The fructose-fed group had higher plasma TBARS and higher urinary TBARS excretion compared to the starch-fed group, suggesting increased production of these substances from lipid peroxidation in vivo. Heart homogenates were less protected against lipid peroxidation in vitro and the lower vitamin E/TG ratio in fructose-fed rats than that in starch-fed rats suggests increased TG-rich lipoprotein susceptibility to lipid peroxidation (33). The interaction of dietary fructose with copper has received considerable attention, and the pro-oxidant effect of fructose has been discussed in relation to decreased copper status and decreased superoxide dismutase activity (8). Although there are discrepancies among the rat experiments, the results indicate that compared with starch fructose exerts a negative effect on copper absorption and/or utilization (34). However, it has not been clearly established from absorption or utilization which step is altered. The results of the present experiment confirmed that fructose feeding in rats is associated with decreased copper status.
It is noteworthy that OFS supplementation results in protection against the pro-oxidant effect of fructose, as shown by decreased plasma TBARS and urinary TBARS excretion in the F/OFS group compared with the S/OFS group. Moreover, the F/OFS group had a lower susceptibility of heart tissue to lipid peroxidation. To the best of our knowledge no antioxidant effect of OFS, or more generally of nondigestible carbohydrates, has yet been described. Whether the modification in lipid metabolism resulting from OFS feeding could counteract the effect of fructose on oxidative stress is unknown. Given the functional properties of OFS, some events occurring in the gastrointestinal tract after OFS feeding could be involved in the antioxidant effect. Results of the present experiment suggest that OFS may affect the availability of carbohydrates. The fact that OFS supplementation tends to lessen the hyperinsulinemic effect of fructose is in agreement with this hypothesis. Because fructose per se does not stimulate insulin secretion by the pancreatic islet, the hyperinsulinemia in fructose-fed rats must result from the developed insulin resistance (35). The reduced plasma leptin level in the F/OFS group is consistent with a possible improvement of the fructose-induced insulin resistance and/or hyperinsulinemia, given that improvement by PPAR- activators of diet-induced insulin resistance and alteration of lipid metabolism are accompanied by reduced plasma leptin concentrations (36). A putative mediator of the effect of OFS could be the products of fermentation, which are known to regulate cellular metabolism.
Moreover, we cannot exclude a direct antioxidant effect of fermentation products, that is, butyrate (37). Finally, OFS supplementation affects mineral metabolism (38), although it is unclear how impairment of antioxidant defense might be related to the effect of fructose on copper metabolism. The present experiment indicates that OFS supplementation was accompanied by normalization of copper status. Previous studies showed that OFS prevented pathology induced by partial copper deficiency in rats fed a high fructose diet (38). The mechanism for the effect of OFS on copper status and severity of copper deficiency among rats fed different carbohydrates (starch or fructose) is unknown. It has been suggested that OFS exerts its beneficial effect through metabolic regulation rather than through enhancing copper absorption (38). The results also confirm the beneficial effects of OFS supplementation on lipid metabolism. Furthermore, as shown by plasma insulin concentration, assessment of insulin resistance delayed by OFS supplementation is of future interest. Whatever the mechanism, further research is needed to define more clearly the protective effect of OFS supplementation against the pro-oxidant effect of fructose.
Special attention should be paid when considering the potential consequences of increased consumption of fructose combined with the low intake of dietary antioxidants in industrialized countries, particularly in relation to the development of the cluster of metabolic abnormalities designated as syndrome X. Potential nutritional benefits of OFS supplementation in fructose-rich diets are suggested by the present results.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Manuscript received 7 January 2003. Initial review completed 13 February 2003. Revision accepted 7 March 2003.
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0.05. P-value, two-way ANOVA. Ch, carbohydrate; OFS, oligofructose.