Centre de Recherche en Nutrition Humaine d‘Auvergne, Unité des Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 Saint‐Genès‐Champanelle, France.
- Key words: Magnesium, fructose, triglyceride, oxidative stress, cardiovascular risk
- Page(s) : 7-12
- Published in: 2003
The purpose of this study was to assess whether dietary carbohydrate could differentially influence the consequences of magnesium deficiency with particular emphasis on lipid metabolism and oxidative stress. Rats were fed a sucrose based or starch based diet either adequate or deficient in magnesium for two weeks. Magnesium deficient rats, as compared with rats fed magnesium adequate diets, displayed the usual decrease in plasma magnesium concentration. The classic symptoms of inflammation including hyperaemia, increased number of blood leukocytes and enlarged spleen weight were observed in these rats. Plasma TG and plasma apo B concentrations were also significantly increased. In addition, magnesium‐deficient animals presented an increased susceptibility to lipid peroxidation of heart and liver tissues as shown by TBARS concentration. Regardless of magnesium status, sucrose feeding did not affect the magnesium plasma level and inflammatory parameters. Feeding rats the sucrose diets induced hypertriglyceridaemia and increased plasma apo B concentration. Heart and liver susceptibility to lipid peroxidation were significantly increased in rats fed the sucrose diets as compared with those fed the starch diets. Sucrose feeding in magnesium deficient rats was associated with higher plasma triglycerides concentration and higher tissue susceptibility to peroxidation as compared with magnesium deficient rats fed the starch diet. The results emphasised the potential detrimental and additional effect of sucrose feeding and magnesium deficiency on cardiovascular risk. Since the intake of magnesium has been reduced appreciably in industrialised countries while fructose consumption has been rapidly increased, the impact of this eating pattern should be clarified in humans.