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首页> 外文期刊>Endocrinology >Activation of hepatic inflammatory pathways by catecholamines is associated with hepatic insulin resistance in male ischemic stroke rats
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Activation of hepatic inflammatory pathways by catecholamines is associated with hepatic insulin resistance in male ischemic stroke rats

机译：儿茶酚胺激活肝炎性途径与雄性缺血性中风大鼠肝胰岛素抵抗有关

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Patients who experience acute ischemic stroke may develop hyperglycemia, even in the absence of diabetes. In the current study we determined the effects of acute stroke on hepatic insulin signaling, TNF-α expression, endoplasmic reticulum (ER) stress, the activities of c-Jun N-terminal kinase (JNK), inhibitor κB kinase β (IKK-β), and nuclear factor-κB (NF-κB) pathways. Rats with cerebral ischemia developed higher blood glucose, and insulin levels, and insulin resistance index, as well as hepatic gluconeogenic enzyme expression compared with the sham-treated group. The hepatic TNF-α mRNA and protein levels were elevated in stroke rats in association with increased ER stress, phosphorylation of JNK1/2 and IKK-β proteins, IκB/NF-κB signaling, and phosphorylation of insulin receptor-1 (IRS-1) at serine residue. The basal and insulin-stimulated tyrosine phosphorylation of IRS-1 and AKT proteins was reduced. In addition, acute stroke increased circulating catecholamines in association with hepatic adrenergic signaling activation. After administration of a nonselective β-adrenergic receptor blocker (propranolol) before induction of cerebral ischemic injury, hepatic adrenergic transduction, TNF-α expression, ER stress, and the activation of the JNK1/2, IKK-β, and NF-κB pathways, and serine phosphorylation of IRS-1 were all attenuated. In contrast, the phosphorylated IRS-1 at tyrosine site and AKT levels were partially restored with improved poststroke hyperglycemia and insulin resistance index. These results suggest that acute ischemic stroke can activate proinflammatory pathways in the liver by the catecholamines and is associated with the development of hepatic insulin resistance.
机译：即使没有糖尿病，经历急性缺血性中风的患者也可能出现高血糖。在本研究中，我们确定了急性中风对肝胰岛素信号传导，TNF-α表达，内质网（ER）应激，c-Jun N末端激酶（JNK）活性，抑制剂κB激酶β（IKK-β ）和核因子-κB（NF-κB）途径。与假治疗组相比，脑缺血大鼠的血糖，胰岛素水平，胰岛素抵抗指数以及肝糖原异生酶的表达更高。脑卒中大鼠肝脏TNF-αmRNA和蛋白水平升高，与内质网应激增加，JNK1 / 2和IKK-β蛋白磷酸化，IκB/NF-κB信号传导以及胰岛素受体1（IRS-1磷酸化）相关）的丝氨酸残基。 IRS-1和AKT蛋白的基础和胰岛素刺激的酪氨酸磷酸化降低。另外，急性中风增加了与肝肾上腺素信号传导相关的循环儿茶酚胺。服用非选择性β-肾上腺素受体阻滞剂（普萘洛尔）后，诱发脑缺血性损伤，肝肾上腺素能传导，TNF-α表达，ER应激以及JNK1 / 2，IKK-β和NF-κB途径的激活，和IRS-1的丝氨酸磷酸化均减弱。相反，酪氨酸位点的磷酸化IRS-1和AKT水平被部分恢复，改善了中风后高血糖症和胰岛素抵抗指数。这些结果表明，急性缺血性中风可以通过儿茶酚胺激活肝脏中的促炎途径，并且与肝胰岛素抵抗的发展有关。

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