Medical Biochemistry Department, Faculty of Medicine, Tanta University, Egypt.
Diabetol Metab Syndr. 2011 Aug 3;3(1):17. doi: 10.1186/1758-5996-3-17.
Obesity has become a leading global health problem owing to its strong association with a high incidence of diseases.
To induce rat obesity using high fat diet (HFD) and to estimate oxidative stress markers in their liver, heart and kidney tissues in order to shed the light on the effect of obesity on these organs.
Sixty white albino rats weighing 150-200 g were randomly divided into two equal groups; group I: received high fat diet for 16 weeks, and group II (control group): received only normal diet (rat chow) for 16 weeks. Blood samples were taken for measurement of lipid profile, tissue samples from liver, heart and kidney were taken for determination of malondialdehyde (MDA), protein carbonyl (PCO), reduced glutathione (GSH) levels, and the activities of glutathione S- transferase (GST) glutathione peroxidase (GPx), catalase (CAT) and paraoxonase1 (PON1) enzymes.
Data showed that feeding HFD diet significantly increased final body weight and induced a state of dyslipideamia. Also our results showed a significant increase MDA and PCO levels in the hepatic, heart and renal tissues of obese rats, as well as a significant decrease in the activity of GST, GPx and PON 1 enzymes. On the other hand CAT enzyme activity showed significant decrease only in renal tissues of obese rats with non significant difference in hepatic and heart tissues. GSH levels showed significant decrease in both renal and hepatic tissues of obese animals and significant increase in their heart tissues. Correlation studies in obese animals showed a negative correlation between MDA and PCO tissue levels and the activities of GPx, GST and PON1 in all tissues and also with CAT enzyme activity in renal tissues. Also a negative correlation was detected between MDA & PCO tissues levels and GSH levels in both hepatic and renal tissues. While positive correlation was found between them and GSH levels in heart tissues.
High fat diet-induced obesity is accompanied by increased hepatic, heart, and renal tissues oxidative stress, which is characterized by reduction in the antioxidant enzymes activities and glutathione levels, that correlate with the increase in MDA and PCO levels in most tissues. This may probably contribute to the additional progression of obesity related problems.
肥胖已成为一个主要的全球健康问题，因为它与许多疾病的高发率密切相关。
使用高脂肪饮食（HFD）诱导大鼠肥胖，并评估其肝脏、心脏和肾脏组织中的氧化应激标志物，以阐明肥胖对这些器官的影响。
将 60 只体重在 150-200g 之间的白色白化大鼠随机分为两组；第 I 组：接受高脂肪饮食 16 周；第 II 组（对照组）：接受正常饮食（大鼠饲料）16 周。采集血样测量血脂谱，采集肝脏、心脏和肾脏组织样本测定丙二醛（MDA）、蛋白羰基（PCO）、还原型谷胱甘肽（GSH）水平以及谷胱甘肽 S-转移酶（GST）、谷胱甘肽过氧化物酶（GPx）、过氧化氢酶（CAT）和对氧磷酶 1（PON1）的活性。
数据显示，给予高脂肪饮食显著增加了最终体重并导致了血脂异常状态。我们的结果还显示，肥胖大鼠肝、心、肾组织中 MDA 和 PCO 水平显著升高，GST、GPx 和 PON1 酶活性显著降低。另一方面，CAT 酶活性仅在肥胖大鼠的肾脏组织中显著降低，而在肝脏和心脏组织中无显著差异。GSH 水平在肥胖动物的肾脏和肝脏组织中均显著降低，而在心脏组织中显著升高。肥胖动物的相关性研究显示，所有组织中 MDA 和 PCO 组织水平与 GPx、GST 和 PON1 的活性呈负相关，与肾脏组织中的 CAT 酶活性也呈负相关。此外，还检测到 MDA 和 PCO 组织水平与肝、肾组织中的 GSH 水平呈负相关，而与心脏组织中的 GSH 水平呈正相关。
高脂肪饮食诱导的肥胖伴随着肝、心、肾组织氧化应激的增加，其特征是抗氧化酶活性和 GSH 水平降低，与大多数组织中 MDA 和 PCO 水平的增加相关。这可能有助于肥胖相关问题的进一步发展。
