Gao Wanxia, Li Xueli, Gao Zhonghong, Li Hailing
School of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, Wuhan, 430074, China.
Biol Trace Elem Res. 2014 Sep;160(3):368-75. doi: 10.1007/s12011-014-0021-9. Epub 2014 Jul 6.
Diabetic nephropathy is both a common and a severe complication of diabetes mellitus. Iron is an essential trace element. However, excess iron is toxic, playing a role in the pathogenesis of diabetic nephropathy. The present study aimed to determine the extent of the interaction between iron and type 2 diabetes in the kidney. Male rats were randomly assigned into four groups: control, iron (300-mg/kg iron dextran), diabetes (a single dose of intraperitoneal streptozotocin), and iron + diabetes group. Iron supplementation resulted in a higher liver iron content, and diabetic rats showed higher serum glucose compared with control rats, which confirmed the model as iron overload and diabetic. It was found that iron + diabetes group showed a greater degree of kidney pathological changes, a remarkable reduction in body weight, and a significant increase in relative kidney weight and iron accumulation in rat kidneys compared with iron or diabetes group. Moreover, malondialdehyde values in the kidney were higher in iron + diabetes group than in iron or diabetes group, sulfhydryl concentration and glutathione peroxidase activity were decreased by the diabetes and iron + diabetes groups, and protein oxidation and nitration levels were higher in the kidney of iron + diabetes group as compared to iron or diabetes group. However, iron supplementation did not elevate the glucose level of a diabetic further. These results suggested that iron increased the diabetic renal injury probably through increased oxidative/nitrative stress and reduced antioxidant capacity instead of promoting a rise in blood sugar levels; iron might be a potential cofactor of diabetic nephropathy, and strict control of iron would be important under diabetic state.
糖尿病肾病是糖尿病常见且严重的并发症。铁是一种必需的微量元素。然而，铁过量具有毒性，在糖尿病肾病的发病机制中起作用。本研究旨在确定铁与2型糖尿病在肾脏中的相互作用程度。雄性大鼠被随机分为四组：对照组、铁（300mg/kg右旋糖酐铁）组、糖尿病组（单次腹腔注射链脲佐菌素）和铁+糖尿病组。补充铁导致肝脏铁含量升高，与对照组相比，糖尿病大鼠血糖更高，这证实了该模型为铁过载和糖尿病模型。研究发现，与铁组或糖尿病组相比，铁+糖尿病组大鼠肾脏病理变化程度更大，体重显著降低，相对肾脏重量显著增加，肾脏铁蓄积增加。此外，铁+糖尿病组肾脏丙二醛值高于铁组或糖尿病组，糖尿病组和铁+糖尿病组的巯基浓度和谷胱甘肽过氧化物酶活性降低，与铁组或糖尿病组相比，铁+糖尿病组肾脏蛋白质氧化和硝化水平更高。然而，补充铁并未进一步提高糖尿病大鼠的血糖水平。这些结果表明，铁可能通过增加氧化/硝化应激和降低抗氧化能力而非促进血糖升高来加重糖尿病肾脏损伤；铁可能是糖尿病肾病的潜在辅助因素，在糖尿病状态下严格控制铁摄入很重要。
