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首页> 外文期刊>Physiological Reports >Renal iron overload in rats with diabetic nephropathy
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Renal iron overload in rats with diabetic nephropathy

机译：糖尿病肾病大鼠肾脏铁超负荷

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AbstractDiabetic nephropathy (DN) remains incurable and is the main cause of end-stage renal disease. We approached the pathophysiology of DN with systems biology, and a comprehensive profile of renal transcripts was obtained with RNA-Seq in ZS (F1 hybrids of Zucker and spontaneously hypertensive heart failure) rats, a model of diabetic nephropathy. We included sham-operated lean control rats (LS), sham-operated diabetic (DS), and diabetic rats with induced renal ischemia (DI). Diabetic nephropathy in DI was accelerated by the single episode of renal ischemia. This progressive renal decline was associated with renal iron accumulation, although serum and urinary iron levels were far lower in DI than in LS. Furthermore, obese/diabetic ZS rats have severe dyslipidemia, a condition that has been linked to hepatic iron overload. Hence, we tested and found that the fatty acids oleic acid and palmitate stimulated iron accumulation in renal tubular cells in vitro. Renal mRNAs encoding several key proteins that promote iron accumulation were increased in DI. Moreover, renal mRNAs encoding the antioxidant proteins superoxide dismutase, catalase, and most of the glutathione synthetic system were suppressed, which would magnify the prooxidant effects of renal iron loads. Substantial renal iron loads occur in obese/diabetic rats. We propose that in diabetes, specific renal gene activation is partly responsible for iron accumulation. This state might be further aggravated by lipid-stimulated iron uptake. We suggest that progressive renal iron overload may further advance renal injury in obese/diabetic ZS rats.
机译：摘要糖尿病肾病（DN）仍然是无法治愈的疾病，是终末期肾脏疾病的主要原因。我们通过系统生物学方法来研究DN的病理生理，并使用RNA-Seq在ZS（Zucker和自发性高血压心力衰竭的F 1 杂种）大鼠（一种糖尿病模型）中获得了肾脏转录物的全面概况肾病。我们包括假手术的瘦身对照大鼠（LS），假手术的糖尿病（DS）和患有诱导性肾缺血的糖尿病大鼠（DI）。单发性肾脏缺血会加速DI中的糖尿病肾病。尽管DI中的血清和尿铁水平远低于LS，但这种进行性肾脏功能下降与肾铁蓄积有关。此外，肥胖/糖尿病ZS大鼠患有严重的血脂异常，这种疾病与肝铁超负荷有关。因此，我们测试并发现脂肪酸油酸和棕榈酸酯在体外刺激肾小管细胞中铁的积累。在DI中，编码几种促进铁积累的关键蛋白的肾mRNA增加。此外，编码抗氧化剂蛋白超氧化物歧化酶，过氧化氢酶和大多数谷胱甘肽合成系统的肾脏mRNA被抑制，这将放大肾铁负荷的促氧化作用。肥胖/糖尿病大鼠发生大量肾铁负荷。我们建议在糖尿病中，特定的肾脏基因激活部分负责铁的积累。脂质刺激的铁摄取可能会进一步加剧这种状态。我们建议进行性肾铁超负荷可能进一步加剧肥胖/糖尿病ZS大鼠的肾脏损伤。

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