Nutrition Department, Faculty of Medicine, University of Chile, Santiago, Chile; Lipid Center, Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile.
Lipid Center, Institute of Nutrition and Food Technology (INTA), University of Chile, Santiago, Chile.
Nutrition. 2018 Jan;45:49-58. doi: 10.1016/j.nut.2017.07.007. Epub 2017 Jul 17.
Iron is involved in processes involving oxygen transfer and utilization. Excess iron is linked to cardiovascular diseases and some types of cancer. Iron overload is associated with oxidative stress development, and may have important interactions with lipid metabolism in the liver favoring the development and progression of non-alcoholic fatty liver disease. The aim of the study described here was to assess the effect of high intake of iron on oxidative stress-related parameters, lipid metabolism, and levels of long-chain polyunsaturated fatty acids (LCPUFAs) in liver and other tissues of the rat.
Male Wistar rats (21 d old) were fed an iron-rich diet (200 mg iron/kg diet, IRD) versus a control diet (50 mg iron/kg diet; CD) for 21 d. Samples of erythrocytes, liver, adipose tissue, brain, heart, and testicles were evaluated for fatty acid composition and hepatic biochemical and oxidative stress parameters, Δ-6 and Δ-5 desaturase activities, SREBP-1c and PPAR-α mRNA expression and DNA-binding capacity, and lipolytic, lipogenic, and antioxidant enzymatic activities.
The IRD caused liver steatosis and increased activity of plasma transaminases, with higher oxidative stress status in plasma and liver. Liver Δ-6 and Δ-5 desaturase exhibited decreased activity, but enhanced expression in response to the IRD compared with the CD, with lower levels of ω-3 and ω-6 LCPUFAs and higher expression and DNA binding of SREBP-1c, whereas expression and DNA-binding activity of PPAR-α were diminished.
IRD induced oxidative stress and a reduction in the desaturation capacity of the liver, with LCPUFA depletion in the different tissues studied, thus promoting a pro-steatotic condition in the liver.
铁参与涉及氧转移和利用的过程。过量的铁与心血管疾病和某些类型的癌症有关。铁过载与氧化应激的发展有关，并且可能与肝脏脂质代谢有重要的相互作用，有利于非酒精性脂肪肝疾病的发展和进展。本研究旨在评估高铁摄入对氧化应激相关参数、脂质代谢以及肝脏和其他组织中长链多不饱和脂肪酸（LCPUFA）水平的影响。
雄性 Wistar 大鼠（21 天大）喂食富含铁的饮食（200mg 铁/千克饮食，IRD）与对照饮食（50mg 铁/千克饮食；CD）21 天。评估红细胞、肝脏、脂肪组织、大脑、心脏和睾丸的脂肪酸组成以及肝生化和氧化应激参数、Δ-6 和 Δ-5 去饱和酶活性、SREBP-1c 和 PPAR-α mRNA 表达和 DNA 结合能力以及脂肪分解、脂肪生成和抗氧化酶活性。
IRD 导致肝脂肪变性和血浆转氨酶活性升高，血浆和肝脏的氧化应激状态更高。与 CD 相比，IRD 下肝脏 Δ-6 和 Δ-5 去饱和酶活性降低，但表达增强，导致 ω-3 和 ω-6 LCPUFA 水平降低，SREBP-1c 表达和 DNA 结合增加，而 PPAR-α 的表达和 DNA 结合活性降低。
IRD 诱导氧化应激和肝脏去饱和能力降低，不同研究组织中的 LCPUFA 耗竭，从而促进肝脏发生脂肪变性。
