Milagro Fermín I, Campión Javier, Martínez J Alfredo
Department of Physiology and Nutrition, University of Navarra, C/Irunlarrea s/n, 31008 Pamplona, Spain.
Obesity (Silver Spring). 2006 Jul;14(7):1118-23. doi: 10.1038/oby.2006.128.
To assess the effects of high-fat feeding on white adipose tissue gene expression and liver oxidative stress.
Male Wistar rats were fed on standard pelleted or high-fat diet to produce a diet-induced obesity model. Therefore, body composition, serum biochemical values and liver malondialdehyde (MDA) were determined after 56 days of feeding. Expression (mRNA) values of three genes were also determined by reverse transcriptase-polymerase chain reaction in white adipose tissue.
Animals fed on the high-fat diet showed more body weight, higher fat deposition and total liver weight, and increased energy intake compared with those on the standard-fat diet. Serum fasting measurements (glucose, insulin, leptin) and homeostasis model assessment insulin resistance index were significantly increased by the high-fat diet consumption. As an indicator of oxidative stress, peroxide decomposition in liver was analyzed, showing an increase of MDA concentrations in rats fed on high-fat diet in comparison with control rats. Interestingly, liver MDA levels correlated positively with body weight gain, serum leptin, and homeostasis model assessment. Finally, leptin and glycerol-3-phosphate dehydrogenase mRNA levels, but not fatty acid synthase, were increased by high-fat diet in comparison with the control-fed group.
These results show a link among increased fat depots, insulin resistance, and liver oxidative stress. Thus, liver oxidative stress probably contributes to hepatic disorders and aggravates the metabolic syndrome, which is accompanied by a stimulation of the esterification of fatty acids as measured by glycerol-3-phosphate dehydrogenase in the adipose tissue, providing support to the hypothesis that not only calories count in the induction of weight gain or metabolic syndrome and that other factors such as oxidative stress may be involved.
评估高脂喂养对白色脂肪组织基因表达和肝脏氧化应激的影响。
雄性Wistar大鼠分别给予标准颗粒饲料或高脂饮食，以建立饮食诱导的肥胖模型。因此，在喂养56天后测定身体组成、血清生化值和肝脏丙二醛（MDA）。还通过逆转录聚合酶链反应测定白色脂肪组织中三个基因的表达（mRNA）值。
与标准脂肪饮食组相比，高脂饮食组动物体重更高、脂肪沉积和肝脏总重量更大，能量摄入增加。高脂饮食导致血清空腹测量值（葡萄糖、胰岛素、瘦素）和稳态模型评估胰岛素抵抗指数显著升高。作为氧化应激的指标，分析了肝脏中的过氧化物分解，结果显示高脂饮食组大鼠的MDA浓度高于对照大鼠。有趣的是，肝脏MDA水平与体重增加、血清瘦素和稳态模型评估呈正相关。最后，与对照组相比，高脂饮食使瘦素和甘油-3-磷酸脱氢酶mRNA水平升高，但脂肪酸合酶mRNA水平未升高。
这些结果表明脂肪储存增加、胰岛素抵抗和肝脏氧化应激之间存在联系。因此，肝脏氧化应激可能导致肝脏疾病并加重代谢综合征，同时伴随着脂肪组织中甘油-3-磷酸脱氢酶所测量的脂肪酸酯化作用增强，这为以下假设提供了支持：在体重增加或代谢综合征的诱导过程中，不仅热量起作用，其他因素如氧化应激也可能参与其中。
