Effect of trivalent chromium on erythropoietin production and the prevention of insulin resistance in HepG2 cells
Effect of trivalent chromium on erythropoietin production and the prevention of insulin resistance in HepG2 cells
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三价铬对 HepG2 细胞促红细胞生成素生成和预防胰岛素抵抗的影响
DOI：
10.1016/j.abb.2021.108960
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发表时间：
2021
影响因子：
3.9
通讯作者：
Nakagawa Hiroshi
中科院分区：
文献类型：
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作者：
Nishimura Kazuhiko;Iitaka Suzuka;Nakagawa Hiroshi
在产生促红细胞生成素（EPO）的 HepG2 细胞中，我们研究了三价铬（Cr）对促进 EPO 产生和诱导胰岛素抵抗的作用。 Cr 增加 HepG2 细胞中缺氧诱导因子 (HIF)-1α 蛋白、EPO mRNA 表达和 EPO 蛋白水平。 Cr 对 EPO 产生的影响可通过抑制增殖物激活受体 γ (PPARγ) 来抑制。通过用补充有棕榈酸的胰岛素抵抗诱导培养基培养 24 小时来诱导胰岛素抵抗。当培养基中添加Cr时，葡萄糖-6-磷酸酶和磷酸烯醇丙酮酸羧激酶1 mRNA表达水平的增加以及磷酸化Akt与Akt蛋白的比率的降低被抑制，并且阻止了胰岛素抵抗的诱导。当PPARγ抑制剂或siPPARγ与Cr一起添加时，Cr对诱导胰岛素抵抗的抑制作用消失。此外，siEPO预处理抑制了EPO mRNA表达的增加，并且Cr的添加对诱导胰岛素抵抗的抑制作用显着降低。这些结果表明，除了其他 PPARγ 介导的活性之外，Cr 在 HepG2 细胞中抑制胰岛素抵抗诱导还涉及促进 PPARγ 介导的 EPO 产生。
In erythropoietin (EPO)-producing HepG2 cells, we investigated the effect of trivalent chromium (Cr) on the promotion of EPO production and the induction of insulin resistance. Cr increased hypoxia-inducible factor (HIF)-1α protein, EPO mRNA expression and EPO protein levels in HepG2 cells. The effect of Cr on EPO production was inhibited by inhibition of proliferator-activated receptor γ (PPARγ). Insulin resistance was induced by culturing with insulin resistance induction medium supplemented with palmitic acid for 24 h. When Cr was added to the medium, the increase inglucose-6-phosphataseandphosphoenolpyruvate carboxykinase1 mRNA expression levels and the decrease in the ratio of phosphorylated Akt to Akt protein were suppressed, and the induction of insulin resistance prevented. When a PPARγ inhibitor or siPPARγ was added together with Cr, the inhibitory effect of Cr on the induction of insulin resistance disappeared. In addition, pretreatment with siEPO suppressed the increase in EPO mRNA expression, and the inhibitory effect on the induction of insulin resistance due to the addition of Cr was significantly reduced. These results suggest that the inhibition of insulin resistance induction by Cr in HepG2 cells involves the promotion of EPO production mediated by PPARγ, in addition to other PPARγ-mediated activities.