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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Interleukin-6 response to insulin-induced hypoglycemia is associated with hypothalamic-pituitary-adrenal axis activation
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Interleukin-6 response to insulin-induced hypoglycemia is associated with hypothalamic-pituitary-adrenal axis activation

机译：白细胞介素-6对胰岛素诱导的低血糖的反应与下丘脑 - 垂体 - 肾上腺轴激活有关

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Increased plasma levels of interleukin-6 (IL-6) in response to acute hypoglycemia have been well documented. Aiming to study the interaction between IL-6 and counter-regulatory hormones during hypoglycemic stress we conducted an exploratory single center study involving 26 adult patients undergoing insulin tolerance test. Insulin-induced hypoglycemia elicited a significant dynamic response of IL-6, adrenaline, noradrenaline, GH, pmlactin, ACTH and serum and salivary cortisol (P < 0.001 for all variables). Patients with insufficient HPA axis response had lower hypoglycemia-induced IL-6 increase (median: 0.88 pg/mL) compared with individuals with intact HPA axis response (2.03 pg/mL, P = 0.007). IL-6 maximal increase correlated with the maximal increase of serum cortisol (r(s) = 0.48; P = 0.013), salivary cortisol (r(s) = 0.66; P = 0.012), plasma ACTH (r(s) = 0.48; P = 0.013) and with the increase in procedure-related symptoms of anxiety and hypoglycemia (r(s) = 0.57; P = 0.003). In conclusion, hypoglycemic stress-induced IL-6 increase is associated with activation of the HPA axis, suggesting that IL-6 response to hypoglycemic stress may be regarded as part of the counter-regulatory response, possibly contributing to the maintenance of glucose homeostasis.
机译：急性低血糖引起的血浆白细胞介素-6（IL-6）水平升高已被充分证明。为了研究低血糖应激期间IL-6和反调节激素之间的相互作用，我们进行了一项探索性单中心研究，涉及26名接受胰岛素耐受试验的成年患者。胰岛素诱导的低血糖引起IL-6、肾上腺素、去甲肾上腺素、GH、pmlactin、ACTH以及血清和唾液皮质醇的显著动态反应（所有变量均P<0.001）。与HPA轴反应正常（2.03 pg/mL，P=0.007）的患者相比，HPA轴反应不足的患者低血糖诱导的IL-6升高较低（中位数：0.88 pg/mL）。IL-6的最大升高与血清皮质醇的最大升高相关（r（s）=0.48；唾液皮质醇（r（s）=0.66；P=0.012），血浆ACTH（r（s）=0.48；P=0.013），随着手术相关焦虑和低血糖症状的增加（r（s）=0.57；P=0.003）。总之，低血糖应激诱导的IL-6升高与HPA轴的激活有关，表明IL-6对低血糖应激的反应可能被视为反调节反应的一部分，可能有助于维持葡萄糖稳态。

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