Razavi Nematollahi Laleh, Kitabchi Abbas E, Stentz Frankie B, Wan Jim Y, Larijani Bagher A, Tehrani Mohammad Mohajer, Gozashti Mohammad Hossein, Omidfar Kobra, Taheri Eghbal
The University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Metabolism. 2009 Apr;58(4):443-8. doi: 10.1016/j.metabol.2008.10.018.
Hyperglycemic crises of diabetic ketoacidosis and nonketotic hyperglycemia are associated with elevation of counterregulatory hormones and proinflammatory cytokines, markers of lipid peroxidation, and oxidative stress. To investigate if other conditions besides hyperglycemia could evoke such a prompt increase in cytokine levels, lipid peroxidation, and oxidative stress markers, we induced hypoglycemic stress by standard insulin tolerance test and measured proinflammatory cytokines, markers of lipid peroxidation, reactive oxygen species (ROS), and counterregulatory hormones. Insulin tolerance test was performed in 13 healthy male subjects with no history of infection, cardiovascular risk factors, or abnormal glucose. At baseline and at 30, 45, 60, 120, and 240 minutes after insulin injection, the following parameters were measured: glucose, cortisol, corticotropin, epinephrine (EP), norepinephrine (NE), growth hormone, tumor necrosis factor (TNF)-alpha, interleukin (IL) 1beta, IL-6, IL-8, free fatty acids, white blood cells, lipid peroxidation markers by thiobarbituric acid assay, and ROS by dichlorofluorescein method. The peak value of white blood cell count at 120 minutes was significantly associated with the peak values of NE at 30 minutes and cortisol at 60 minutes. By comparing the area under the curve of measured parameters, EP emerged as significant predictor of TNF-alpha (P = .05) and IL-8 (P = .027). Cortisol emerged as predictor of IL-1beta significantly (P = .05). Corticotropin predicted area under the curve of IL-6 with borderline significance (P = .06). In the present study, insulin-induced hypoglycemia in nondiabetic male subjects is associated with increased proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IL-8), markers of lipid peroxidation, ROS, and leukocytosis. Elevations of NE, EP, corticotropin, and cortisol in hypoglycaemia are associated with the elevation of the proinflammatory cytokines and leukocytosis.
糖尿病酮症酸中毒和非酮症高血糖的高血糖危象与升糖调节激素、促炎细胞因子、脂质过氧化标志物及氧化应激的升高有关。为了研究除高血糖外的其他情况是否会引发细胞因子水平、脂质过氧化和氧化应激标志物如此迅速的升高，我们通过标准胰岛素耐量试验诱导低血糖应激，并测量促炎细胞因子、脂质过氧化标志物、活性氧（ROS）和升糖调节激素。对13名无感染史、心血管危险因素或血糖异常的健康男性受试者进行胰岛素耐量试验。在胰岛素注射后的基线以及30、45、60、120和240分钟，测量以下参数：血糖、皮质醇、促肾上腺皮质激素、肾上腺素（EP）、去甲肾上腺素（NE）、生长激素、肿瘤坏死因子（TNF）-α、白细胞介素（IL）1β、IL-6、IL-8、游离脂肪酸、白细胞、通过硫代巴比妥酸法测定的脂质过氧化标志物以及通过二氯荧光素法测定的ROS。白细胞计数在120分钟时的峰值与NE在30分钟时的峰值以及皮质醇在60分钟时的峰值显著相关。通过比较测量参数的曲线下面积，EP成为TNF-α（P = 0.05）和IL-8（P = 0.027）的显著预测因子。皮质醇成为IL-1β的显著预测因子（P = 0.05）。促肾上腺皮质激素对IL-6曲线下面积的预测具有临界显著性（P = 0.06）。在本研究中，非糖尿病男性受试者中胰岛素诱导的低血糖与促炎细胞因子（TNF-α、IL-1β、IL-6和IL-8）、脂质过氧化标志物、ROS升高及白细胞增多有关。低血糖时NE、EP、促肾上腺皮质激素和皮质醇的升高与促炎细胞因子升高及白细胞增多有关。
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