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首页> 外文期刊>Clinical and experimental pharmacology & physiology >Protectin DX DX ameliorates palmitate‐induced hepatic insulin resistance through AMPK AMPK / SIRT SIRT 1‐mediated modulation of fetuin‐A and SeP expression
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Protectin DX DX ameliorates palmitate‐induced hepatic insulin resistance through AMPK AMPK / SIRT SIRT 1‐mediated modulation of fetuin‐A and SeP expression

机译：Protectin DX DX通过AMPK AMPK / SIRT SIRT 1介导的胎儿-A和SEP表达调节术后棕榈酸酯诱导的肝胰岛素抵抗力

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Abstract The role as well as the molecular mechanisms of protectin DX ( PDX ) in the prevention of hepatic insulin resistance, a hallmark of type 2 diabetes, remains unknown. Therefore, the present study was designed to explore the direct impact of PDX on insulin resistance and to investigate the expression of fetuin‐A and selenoprotein P (SeP), hepatokines that are involved in insulin signalling, in hepatocytes. Human serum levels of PDX as well as fetuin‐A and SeP were determined by high‐performance liquid chromatography ( HPLC ). Human primary hepatocytes were treated with palmitate and PDX . NF ‐κB phosphorylation as well as expression of insulin signalling associated genes and hepatokines were determined by Western blotting analysis. FOXO 1 binding levels were measured by quantitative real‐time PCR . Selected genes from candidate pathways were evaluated by small interfering (si) RNA ‐mediated gene suppression. Serum PDX levels were significantly ( P? ? 0.05) downregulated, whereas serum fetuin‐A and SeP levels were increased ( P? ? 0.05) in obese subjects compared with healthy subjects. In in vitro experiments, PDX treatment increased AMP ‐activated protein kinase ( AMPK ) phosphorylation and SIRT 1 expression and attenuated palmitate‐induced fetuin‐A and SeP expression and insulin resistance in hepatocytes. AMPK or SIRT 1 si RNA mitigated the suppressive effects of PDX on palmitate‐induced fetuin‐A through NF ‐κB and SeP expression linked to FOXO 1 and insulin resistance. Recombinant fetuin‐A and SeP reversed the suppressive effects of fetuin‐A and SeP expression on palmitate‐mediated impairment of insulin signalling. The current finding provides novel insight into the underlying mechanism linking hepatokines to the pathogenesis of hepatic insulin resistance.
机译：摘要作用以及保护素DX（PDX）在预防肝胰岛素抵抗中的角色，患有2型糖尿病的标志，仍然未知。因此，本研究旨在探讨PDX对胰岛素信号，肝脏信号传导胰岛素信号，肝脏的表达对胰岛素抗性的直接影响。通过高效液相色谱（HPLC）测定人类血清PDX水平和呋喃-A和SEP。用棕榈酸盐和PDX处理人的原发性肝细胞。通过Western印迹分析测定NF-κB磷酸化以及胰岛素信号传导相关基因和肝运动量的表达。通过定量实时PCR测量FOXO 1结合水平。通过小干扰（Si）RNA介导的基因抑制评估来自候选途径的所选基因。下调血清PDX水平（p≤≤0.05），而肥胖的胎儿-A和SEP水平与健康受试者相比，肥胖的受试者中的血清胎儿-A和SEP水平增加（p≤0.05）。在体外实验中，PDX治疗增加了AMP-递除的蛋白激酶（AMPK）磷酸化和SIRT 1表达，并减弱了肝细胞中的棕榈酸盐诱导的胎儿-A和SEP表达和胰岛素抗性。 AMPK或SIRT 1 Si RNA减轻了PDX在与Foxo1和胰岛素抵抗的NF-κB和SEP表达上的PDX对棕榈酸盐诱导的胎素-A的抑制作用。重组胎素-A和SEP逆转了Fetuin-A和SEP表达对棕榈酸酯介导的胰岛素信号传导损伤的抑制作用。目前的发现提供了对将肝电压因子连接到肝胰岛素抵抗力发病机制的潜在机制的新颖洞察力。

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