Peitl Barna, Döbrönte Róbert, Németh József, Mezey Géza, Kovács Péter, Paragh György, Szilvássy Zoltán
Experimental and Clinical Pharmacology Consortium, University of Debrecen, H-4032 Debrecen, Germany.
Metabolism. 2005 May;54(5):579-83. doi: 10.1016/j.metabol.2004.11.014.
The effect of left cervical vagal nerve stimulation was studied on insulin sensitivity to test the proposed permissive insulin-sensitizing role of hepatic vagal parasympathetic efferent pathways in fasted and fed anesthetized rats. In fed animals, electrical stimulation (square impulses: 25 V, 5 Hz, 0.5 milliseconds over 15 minutes) of the vagal nerve induced hyperglycemia and an increase in plasma insulin immunoreactivity. Atropine (1.0 mg/kg intravenously) induced insulin resistance estimated by rapid insulin sensitivity testing. This was amplified when the vagal nerve was stimulated. The insulin-resistant state developed by fasting was not modified by either treatment with atropine or electrical stimulation. We conclude that both parasympathetic cholinergic and noncholinergic vagal efferents modulate postprandial neurogenic insulin sensitivity adjustments.
研究了左颈迷走神经刺激对胰岛素敏感性的影响,以检验所提出的肝迷走神经副交感传出通路在禁食和喂食的麻醉大鼠中允许性胰岛素增敏作用。在喂食的动物中,迷走神经的电刺激(方波脉冲:25V,5Hz,0.5毫秒,持续15分钟)诱导高血糖和血浆胰岛素免疫反应性增加。阿托品(静脉注射1.0mg/kg)通过快速胰岛素敏感性测试诱导胰岛素抵抗。当迷走神经受到刺激时,这种抵抗会增强。禁食诱导的胰岛素抵抗状态不受阿托品治疗或电刺激的影响。我们得出结论,副交感胆碱能和非胆碱能迷走神经传出纤维均调节餐后神经源性胰岛素敏感性调节。