Changes in lipid metabolism and antioxidant defense status in spontaneously hypertensive rats and Wistar rats fed a diet enriched with fructose and saturated fatty acids

被引:53
作者
Girard, A
Madani, S
El Boustani, ES
Belleville, J
Prost, J [1 ]
机构
[1] Univ Bourgogne, UPRES Lipides Nutr, EA 2422, Fac Sci Gabriel, Dijon, France
[2] Univ Caddi Ayyad, Fac Sci Semlalia, Marrakech, Morocco
关键词
fructose; saturated fatty acids; spontaneously hypertensive rats; antioxidant status;
D O I
10.1016/j.nut.2004.04.022
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Objective: Larger doses of fructose and saturated fat have been associated with oxidative stress and development of hypertension. The effects of modest amounts of fructose and saturated fatty acids on oxidative stress are unknown. Methods: To increase knowledge on this question, 10-wk-old spontaneously hypertensive rats and Wistar rats were fed for 8 wk with a control diet or an experimental diet enriched with fructose (18%) and saturated fatty acids (11%; FS diet). The total antioxidant status of organs and red blood cells was assayed by monitoring the rate of free radical-induced red blood cell hemolysis. Sensitivity of very low-density lipoprotein and low-density lipoprotein (VLDL-LDL) to copper-induced lipid peroxidation was determined as the production of thiobarbituric acid-reactive substances. Antioxidant enzymes and vitamins were also measured to establish the oxidative stress effect. Results: The FS diet did not affect blood pressure in either strain, but it increased plasma insulin concentrations only in Wistar rats without affecting those of glucose of either strain. The FS diet significantly enhanced plasma and VLDL-LDL triacylglycerol concentrations without affecting concentrations of VLDL-LDL thiobarbituric acid-reactive substances. The decreased content of arachidonic acid and total polyunsaturated fatty acids in VLDL-LDL by the FS diet may have prevented lipid peroxidation in this fraction. Moreover, FS consumption by both strains was accompanied by a significant increase in total antioxidant capacity of adipose tissue, muscle, heart, and liver. This may have resulted from increased tissue ascorbic acid levels and glutathione peroxidase and glutathione reductase activities in tissues. Conclusions: These findings clearly indicate that the FS diet did not alter blood pressure of spontaneously hypertensive rats and Wistar rats. The FS diet resulted in hypertriglyceridemia but increased the total antioxidant status, which may prevent lipid peroxidation in these rats. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:240 / 248
页数:9
相关论文
共 49 条
[1]   Free radical generators cause changes in endothelial and inducible nitric oxide synthases and endothelin-1 immunoreactivity in endothelial cells from hyperlipidemic rabbits [J].
Aliev, G ;
Bodin, P ;
Burnstock, G .
MOLECULAR GENETICS AND METABOLISM, 1998, 63 (03) :191-197
[2]  
ANDERSON ME, 1985, METHOD ENZYMOL, V113, P548
[3]   A clinical trial of the effects of dietary patterns on blood pressure [J].
Appel, LJ ;
Moore, TJ ;
Obarzanek, E ;
Vollmer, WM ;
Svetkey, LP ;
Sacks, FM ;
Bray, GA ;
Vogt, TM ;
Cutler, JA ;
Windhauser, MM ;
Lin, PH ;
Karanja, N .
NEW ENGLAND JOURNAL OF MEDICINE, 1997, 336 (16) :1117-1124
[4]   Diet-induced insulin resistance precedes other aspects of the metabolic syndrome [J].
Barnard, RJ ;
Roberts, CK ;
Varon, SM ;
Berger, JJ .
JOURNAL OF APPLIED PHYSIOLOGY, 1998, 84 (04) :1311-1315
[5]  
Bergmeyer HU., 1983, METHODS ENZYMATIC AN, VVI., P258, DOI [DOI 10.1016/B978-0-12-091302-2.X5001-4, 10.1016/B978-0-12-091302-2.X5001-4]
[6]   VANADYL SULFATE PREVENTS FRUCTOSE-INDUCED HYPERINSULINEMIA AND HYPERTENSION IN RATS [J].
BHANOT, S ;
MCNEILL, JH ;
BRYERASH, M .
HYPERTENSION, 1994, 23 (03) :308-312
[7]  
Bjorntorp Per, 1994, Current Opinion in Lipidology, V5, P166, DOI 10.1097/00041433-199405030-00003
[8]  
BLACHE D, 1992, LUNAR-BASED CHEMICAL ANALYSIS LABORATORY, P82
[9]  
CORTAS NK, 1990, CLIN CHEM, V36, P1440
[10]   Phosphatidylinositol 3-kinase and p70 S6 kinase participate in the regulation of protein turnover in skeletal muscle by insulin and insulin-like growth factor I [J].
Dardevet, D ;
Sornet, C ;
Vary, T ;
Grizard, J .
ENDOCRINOLOGY, 1996, 137 (10) :4087-4094