Busserolles Jérôme, Gueux Elyett, Rock Edmond, Mazur Andrzej, Rayssiguier Yves
Centre de Recherche en Nutrition Humaine d'Auvergne, Unité des Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 Saint-Genès-Champanelle, France.
Magnes Res. 2003 Mar;16(1):7-12.
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.
本研究的目的是评估膳食碳水化合物是否会对镁缺乏的后果产生不同影响,尤其着重于脂质代谢和氧化应激方面。将大鼠分为两组,分别喂食以蔗糖为基础或淀粉为基础的饮食,且这些饮食的镁含量分别充足或缺乏,持续两周。与喂食镁含量充足饮食的大鼠相比,镁缺乏的大鼠血浆镁浓度出现了常见的降低。在这些大鼠中观察到了炎症的典型症状,包括充血、血液白细胞数量增加和脾脏重量增大。血浆甘油三酯(TG)和血浆载脂蛋白B浓度也显著升高。此外,如丙二醛(TBARS)浓度所示,镁缺乏的动物心脏和肝脏组织对脂质过氧化的敏感性增加。无论镁状态如何,喂食蔗糖均不影响血浆镁水平和炎症参数。给大鼠喂食蔗糖饮食会导致高甘油三酯血症,并增加血浆载脂蛋白B浓度。与喂食淀粉饮食的大鼠相比,喂食蔗糖饮食的大鼠心脏和肝脏对脂质过氧化的敏感性显著增加。与喂食淀粉饮食的镁缺乏大鼠相比,喂食蔗糖的镁缺乏大鼠血浆甘油三酯浓度更高,组织对过氧化的敏感性也更高。结果强调了喂食蔗糖和镁缺乏对心血管风险的潜在有害及额外影响。由于工业化国家中镁的摄入量已明显减少,而果糖消费量迅速增加,这种饮食模式对人类的影响应予以阐明。