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首页> 外文期刊>Cell metabolism >An afferent vagal nerve pathway links hepatic PPARalpha activation to glucocorticoid-induced insulin resistance and hypertension.
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An afferent vagal nerve pathway links hepatic PPARalpha activation to glucocorticoid-induced insulin resistance and hypertension.

机译：迷走神经传入神经通路将肝PPARα激活与糖皮质激素诱导的胰岛素抵抗和高血压联系起来。

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摘要

Glucocorticoid excess causes insulin resistance and hypertension. Hepatic expression of PPARalpha (Ppara) is required for glucocorticoid-induced insulin resistance. Here we demonstrate that afferent fibers of the vagus nerve interface with hepatic Ppara expression to disrupt blood pressure and glucose homeostasis in response to glucocorticoids. Selective hepatic vagotomy decreased hyperglycemia, hyperinsulinemia, hepatic insulin resistance, Ppara expression, and phosphoenolpyruvate carboxykinase (PEPCK) enzyme activity in dexamethasone-treated Ppara(+/+) mice. Selective vagotomy also decreased blood pressure, adrenergic tone, renin activity, and urinary sodium retention in these mice. Hepatic reconstitution of Ppara in nondiabetic, normotensive dexamethasone-treated PPARalpha null mice increased glucose, insulin, hepatic PEPCK enzyme activity, blood pressure, and renin activity in sham-operated animals but not hepatic-vagotomized animals. Disruption of vagal afferent fibers by chemical or surgical means prevented glucocorticoid-induced metabolic derangements. We conclude that a dynamic interaction between hepatic Ppara expression and a vagal afferent pathway is essential for glucocorticoid induction of diabetes and hypertension.
机译：糖皮质激素过多会引起胰岛素抵抗和高血压。肝糖皮质激素诱导的胰岛素抵抗需要PPARalpha（Ppara）的肝表达。在这里，我们证明迷走神经的传入纤维与肝Ppara表达相交联，以响应于糖皮质激素而破坏血压和葡萄糖稳态。选择性肝迷走神经切断术可降低地塞米松治疗的Ppara（+ / +）小鼠的高血糖，高胰岛素血症，肝胰岛素抵抗，Ppara表达和磷酸烯醇丙酮酸羧激酶（PEPCK）酶活性。选择性迷走神经切断术还降低了这些小鼠的血压，肾上腺素能，肾素活性和尿钠retention留。在非糖尿病，血压正常的地塞米松治疗的PPARα无效小鼠中，肝对Ppara的重建增加了假手术动物而非肝迷走神经切断动物的葡萄糖，胰岛素，肝PEPCK酶活性，血压和肾素活性。通过化学或外科手段破坏迷走神经传入纤维可防止糖皮质激素引起的代谢紊乱。我们得出结论，肝Ppara表达与迷走神经传入途径之间的动态相互作用对于糖皮质激素诱发糖尿病和高血压至关重要。

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