Diniz Yeda S, Burneiko Regina M, Seiva Fabio R F, Almeida Flávia Q A, Galhardi Cristiano Machado, Filho José Luiz V B Novelli, Mani Fernanda, Novelli Ethel L B
Department of Chemistry and Biochemistry, Institute of Biological Sciences, São Paulo State University, UNESP, 18618-000 Botucatu, São Paulo, Brazil.
Int J Cardiol. 2008 Feb 20;124(1):92-9. doi: 10.1016/j.ijcard.2006.12.025. Epub 2007 Mar 26.
Diet compounds may influence obesity-related cardiac oxidative stress and metabolic sifting. Carbohydrate-rich diet may be disadvantageous from fat-rich diet to cardiac tissue and glycemic index rather than lipid profile may predict the obesity-related cardiac effects.
Male Wistar rats were divided into three groups (n=8/group): (C) receiving standard chow (3.0 kcal/g); (CRD) receiving carbohydrate-rich diet (4.0 kcal/g), and (FRD) receiving fat-rich diet (4.0 kcal/g). Rats were sacrificed after the oral glucose tolerance test (OGTT) at 60 days of dietary treatments. Lipid profile and oxidative stress parameters were determined in serum. Myocardial samples were used to determine oxidative stress, metabolic enzymes, glycogen and triacylglycerol.
FRD rats showed higher final body weight and body mass index than CRD and C. Serum cholesterol and low-density lipoprotein were higher in FRD than in CRD, while triacylglycerol and oxidized low-density lipoprotein cholesterol were higher in CRD than in FRD. CRD rats had the highest myocardial lipid hydroperoxide and diminished superoxide dismutase and catalase activities. Myocardial glycogen was lower and triacylglycerol was higher in CRD than in C and FRD rats. Although FRD rats had depressed myocardial-reducing power, no significant changes were observed in myocardial energy metabolism. Myocardial beta-hydroxyacyl coenzyme-A dehydrogenase and citrate synthase, as well as the enhanced lactate dehydrogenase/citrate synthase ratio indicated that fatty acid degradation was decreased in CRD rats. Glycemic index was positively correlated with obesity-related cardiac effects.
Isoenergetic carbohydrate-rich and fat-rich diets induced different degree of obesity and differently affected lipid profile. Carbohydrate-rich diet was deleterious relative to fat-rich diet in the heart enhancing lipoperoxidation and shifting the metabolic pathway for energy production. Glycemic index rather than dyslipidemic profile may predict the obesity effects on cardiac tissue.
饮食成分可能影响与肥胖相关的心脏氧化应激和代谢转换。富含碳水化合物的饮食与富含脂肪的饮食相比，对心脏组织可能不利，且血糖指数而非血脂谱可能预测与肥胖相关的心脏效应。
将雄性Wistar大鼠分为三组（每组n = 8）：（C）组给予标准饲料（3.0千卡/克）；（CRD）组给予富含碳水化合物的饮食（4.0千卡/克），以及（FRD）组给予富含脂肪的饮食（4.0千卡/克）。在饮食处理60天后进行口服葡萄糖耐量试验（OGTT），然后处死大鼠。测定血清中的血脂谱和氧化应激参数。心肌样本用于测定氧化应激、代谢酶、糖原和三酰甘油。
FRD组大鼠的最终体重和体重指数高于CRD组和C组。FRD组血清胆固醇和低密度脂蛋白高于CRD组，而CRD组三酰甘油和氧化型低密度脂蛋白胆固醇高于FRD组。CRD组大鼠心肌脂质过氧化氢含量最高，超氧化物歧化酶和过氧化氢酶活性降低。CRD组大鼠心肌糖原低于C组和FRD组大鼠，三酰甘油高于C组和FRD组大鼠。尽管FRD组大鼠心肌还原能力降低，但心肌能量代谢未见明显变化。CRD组大鼠心肌β-羟酰基辅酶A脱氢酶和柠檬酸合酶以及乳酸脱氢酶/柠檬酸合酶比值升高，表明脂肪酸降解减少。血糖指数与肥胖相关的心脏效应呈正相关。
等能量的富含碳水化合物和富含脂肪的饮食诱导不同程度的肥胖，并对血脂谱产生不同影响。相对于富含脂肪的饮食，富含碳水化合物的饮食对心脏有害，会增强脂质过氧化并改变能量产生的代谢途径。血糖指数而非血脂异常谱可能预测肥胖对心脏组织的影响。
