Hostname: page-component-586b7cd67f-rcrh6 Total loading time: 0 Render date: 2024-11-22T22:51:25.414Z Has data issue: false hasContentIssue false
  • English
  • Français

Short-term consumption of a high-sucrose diet has a pro-oxidant effect in rats

Published online by Cambridge University Press:  09 March 2007

Jérôme Busserolles ,
Edmond Rock ,
Elyett Gueux ,
Andrzej Mazur ,
Pascal Grolier  and
Yves Rayssiguier
Jérôme Busserolles
Affiliation:
Centre de Recherche en Nutrition Humaine d'Auvergne, Unité des Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 Saint-Genès-Champanelle, France
Edmond Rock
Affiliation:
Centre de Recherche en Nutrition Humaine d'Auvergne, Unité des Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 Saint-Genès-Champanelle, France
Elyett Gueux
Affiliation:
Centre de Recherche en Nutrition Humaine d'Auvergne, Unité des Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 Saint-Genès-Champanelle, France
Andrzej Mazur
Affiliation:
Centre de Recherche en Nutrition Humaine d'Auvergne, Unité des Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 Saint-Genès-Champanelle, France
Pascal Grolier
Affiliation:
Centre de Recherche en Nutrition Humaine d'Auvergne, Unité des Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 Saint-Genès-Champanelle, France
Yves Rayssiguier*
Affiliation:
Centre de Recherche en Nutrition Humaine d'Auvergne, Unité des Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 Saint-Genès-Champanelle, France
*
*Corresponding author: Dr Y. Rayssiguier, fax +33 473 62 46 38, email [email protected]
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

The underlying mechanisms for the detrimental consequences of a high-fructose diet in animal models are not clear. However, the possibility exists that fructose feeding facilitates oxidative damage. Thus, the aim of the present study was to assess, in weaning rats, the effect of a high-sucrose diet v. starch diet for 2 weeks on oxidative stress variables. Plasma lipid levels were measured and lipid peroxidation was evaluated by urine and plasma thiobarbituric acid-reactive substances (TBARS). The susceptibilities of several tissues to peroxidation were determined in tissue homogenates after in vitro lipid peroxidation. Antioxidant defence variables were evaluated by measuring plasma and heart vitamin E levels, and heart superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities. Higher plasma triacylglycerol (P<0·01) and TBARS (P<0·01) levels were found in rats fed the sucrose diet as compared with the starch-fed group, whereas plasma α-tocopherol levels were significantly decreased in the sucrose-fed group compared with the starch-fed group (P<0·01). Higher urine TBARS (P<0·01) were found in the sucrose-fed group compared with the starch-fed group, suggesting increased production of these substances from lipid peroxidation in vivo. Higher susceptibility to peroxidation in heart, thymus and pancreas was also found in the sucrose-fed group v. the starch-fed group. No statistical differences were observed for liver TBARS level between the two groups. Heart SOD activity was significantly decreased (P<0·001) in the sucrose-fed group compared with the starch-fed group, whereas heart vitamin E level and GPX activity were not different between the groups. However, the in vitro generation of superoxide radical in heart homogenate, measured by electron spin resonance detection and spin trapping, was not increased in the sucrose-fed group compared with starch-fed rats. Altogether, the results indicate that a short-term consumption of a high-sucrose diet negatively affects the balance of free radical production and antioxidant defence in rats, leading to increased lipid susceptibility to peroxidation.

Keywords

High-sucrose dietOxidative stressFree radicalsRats
Type
Research Article
Information
British Journal of Nutrition , Volume 87 , Issue 4 , April 2002 , pp. 337 - 342
Copyright
Copyright © The Nutrition Society 2002

References

Bakker, SJ, Ijzerman, RG, Teerlink, T, Westerhoff, HV, Gans, RO & Heine, RJ (2000) Cytosolic triglycerides and oxidative stress in central obesity: the missing link between excessive atherosclerosis, endothelial dysfunction, and beta-cell failure? Atherosclerosis 148, 17–21.CrossRefGoogle ScholarPubMed
Brooks, BR & Klamerth, OL (1968) Interaction of DNA with bifunctional aldehydes. European Journal of Biochemistry 5, 178–182.CrossRefGoogle ScholarPubMed
Burkitt, MJ & Mason, RP (1991) Direct evidence for in vivo hydroxyl-radical generation in experimental iron overload: an ESR spin-trapping investigation. Proceedings of the National Academy of Sciences, USA 88, 8440–8444.CrossRefGoogle ScholarPubMed
Draper, HH, Polensek, L, Hadley, M & McGirr, LG (1984) Urinary malondialdehyde as an indicator of lipid peroxidation in the diet and in the tissues. Lipids 19, 836–843.CrossRefGoogle ScholarPubMed
Esterbauer, H, Gebicki, J, Puhl, H & Jurgens, G (1992) The role of lipid peroxidation and antioxidants in oxidative modification of LDL. Free Radical Biology and Medicine 13, 341–390.CrossRefGoogle ScholarPubMed
Faure, P, Rossini, E, Lafond, JL, Richard, MJ, Favier, A & Halimi, S (1997) Vitamin E improves the free radical defense system potential and insulin sensitivity of rats fed high fructose diets. Journal of Nutrition 127, 103–107.CrossRefGoogle ScholarPubMed
Fields, M, Ferretti, RJ, Reiser, S & Smith, JC (1984) The severity of copper deficiency in rats is determined by the type of dietary carbohydrates. Proceedings of the Society for Experimental Biology and Medicine 175, 530–537.CrossRefGoogle Scholar
Frayn, KN & Kingman, SM (1995) Dietary sugars and lipid metabolism in humans. American Journal of Clinical Nutrition 62, 250S–263S.CrossRefGoogle ScholarPubMed
Hallfrisch, J (1990) Metabolic effects of dietary fructose. FASEB Journal 4, 2652–2660.CrossRefGoogle ScholarPubMed
Halliwell, B (1996) Oxidative stress, nutrition and health. Experimental strategies for optimization of nutritional antioxidant intake in humans. Free Radical Research 25, 57–74.CrossRefGoogle ScholarPubMed
Henry, RR, Crapo, PA & Thorburn, AW (1991) Current issues in fructose metabolism. Annual Review of Nutrition 11, 21–39.CrossRefGoogle ScholarPubMed
Kritchevsky, D, Davidson, LM, Kim, HK, Krendel, DA, Malhotra, S, Mendelsohn, D, van der Watt, JJ, duPlessis, JP & Winter, PA (1980) Influence of type of carbohydrate on atherosclerosis in baboons fed semi purified diets plus 0·1 % cholesterol. American Journal of Clinical Nutrition 33, 1869–1887.CrossRefGoogle Scholar
Lee, HS, Shoeman, DW & Csallany, AS (1992) Urinary response to in vivo lipid peroxidation induced by vitamin E deficiency. Lipids 27, 124–128.CrossRefGoogle ScholarPubMed
Levi, B & Werman, MJ (1998) Long-term fructose consumption accelerates glycation and several age-related variables in male rats. Journal of Nutrition 128, 1442–1449.CrossRefGoogle ScholarPubMed
McDonald, RB (1995) Influence of dietary sucrose on biological aging. American Journal of Clinical Nutrition 62, 284S–293S.CrossRefGoogle ScholarPubMed
Malpuech-Brugère, C, Nowacki, W, Daveau, M, Gueux, E, Linard, C, Rock, E, Lebreton, JP, Mazur, A & Rayssiguier, Y (2000) Inflammatory response following acute magnesium deficiency in the rat. Biochimica et Biophysica Acta 1501, 91–98.CrossRefGoogle ScholarPubMed
Mamo, JC, Hirano, T, James, L, Szeto, L & Steiner, G (1991) Partial characterization of the fructose-induced defect in very-low-density-lipoprotein triglyceride metabolism. Metabolism 40, 888–893.CrossRefGoogle ScholarPubMed
O'Dell, BL (1993) Fructose and mineral metabolism. American Journal of Clinical Nutrition 58, 771S–778S.CrossRefGoogle ScholarPubMed
Paglia, DE & Valentine, WN (1967) Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. Journal of Laboratory and Clinical Medicine 70, 158–169.Google ScholarPubMed
Paolisso, G, D'Amore, A, Giugliano, D, Ceriello, A, Varricchio, M & D'Onofrio, F (1993) Pharmacologic doses of vitamin E improve insulin action in healthy subjects and non-insulin-dependent diabetic patients. American Journal of Clinical Nutrition 57, 650–656.CrossRefGoogle ScholarPubMed
Rayssiguier, Y, Gueux, E, Bussière, L & Mazur, A (1993) Copper deficiency increases the susceptibility of lipoproteins and tissues to peroxidation in rats. Journal of Nutrition 123, 1343–1348.Google ScholarPubMed
Rayssiguier, Y, Gueux, E & Weiser, D (1981) Effect of magnesium deficiency on lipid metabolism in rats fed a high carbohydrate diet. Journal of Nutrition 111, 1876–1883.CrossRefGoogle ScholarPubMed
Reaven, GM (1988) Banting lecture. Role of insulin resistance in human disease. Diabetes 37, 1595–1607.CrossRefGoogle ScholarPubMed
Reiser, S (1982) Metabolic risk factors associated with heart disease and diabetes in carbohydrate-sensitive humans when consuming sucrose as compared to starch. In Metabolic Effects of Utilisable Dietary Carbohydrates, pp. 239–259 [Reiser, S, editor]. New York–Basel: Marcel Dekker, Inc.Google Scholar
Rice-Evans, CA, Diplock, AT & Symons, MCR [Burdon, RH and van Knippenber, PH, editors]. Amsterdam: Elsevier.Google Scholar
Rock, E, Astier, C, Lab, C, Vignon, X, Gueux, E, Motta, C & Rayssiguier, Y (1995) Dietary magnesium deficiency in rats enhances free radical production in skeletal muscle. Journal of Nutrition 125, 1205–1210.Google ScholarPubMed
Ross, R (1999) Atherosclerosis: An inflammatory disease. New England Journal of Medicine 340, 115–126.CrossRefGoogle ScholarPubMed
Tiedge, M, Lortz, S, Drinkgern, J & Lenzen, S (1997) Relation between antioxidant enzyme gene expression and antioxidant defense status on insulin-producing cells. Diabetes 46, 1733–1742.CrossRefGoogle ScholarPubMed
van Campen, DR & Scaife, PU (1967) Zinc interference with copper absorption in rats. Journal of Nutrition 91, 473–476.CrossRefGoogle ScholarPubMed
Vrana, A & Fabry, P (1983) Metabolic effects of high sucrose or fructose intake. World Review of Nutrition and Dietetics 42, 56–101.CrossRefGoogle ScholarPubMed