Eik W, Marcon S S, Krupek T, Previdelli I T S, Pereira O C N, Silva M A R C P, Bazotte R B
Disciplina de Endocrinologia, Departamento de Medicina, Universidade Estadual de Maringá, Maringá, PR, Brasil.
Programa de Pós Graduação em Ciências da Saúde, Centro de Ciências da Saúde, Universidade Estadual de Maringá, Maringá, PR, Brasil.
Braz J Med Biol Res. 2016 Jul 11;49(8). doi: 10.1590/1414-431X20165195.
We evaluated the impact of postprandial glycemia on blood levels of pro-inflammatory and anti-inflammatory cytokines during an oral glucose tolerance test in non-diabetic patients with symptoms suggesting reactive hypoglycemia. Eleven patients with clinical symptoms suggesting reactive hypoglycemia received an oral glucose solution (75 g) Blood was collected at 0 (baseline), 30, 60, 120 and 180 min after glucose ingestion and the plasma concentrations of interferon-α (IFN-α), interferon-γ (IFN-γ), interleukin-1 receptor antagonist (IL-1RA), interleukin 2 (IL-2), interleukin-2 receptor (IL-2R), interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 8 (IL-8), interleukin 10 (IL-10), interleukin-12 (IL-12), interleukin 13 (IL-13), interleukin 15 (IL-15), interleukin 17 (IL-17), IFN-γ inducible protein 10 (IP-10), monocyte chemotactic protein 1 (MCP1), monokine induced by IFN-γ (MIG), macrophage inflammatory protein-1α (MIP-1α), interleukin-1β (IL-1β), colony stimulating factor (G-CSF), granulocyte-macrophage CSF (GM-CSF), basic fibroblast growth factor (FGF-basic), eotaxin, tumor necrosis factor α (TNFα), epidermal growth factor (EGF), hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), macrophage inflammatory protein-1α (MIP-1α), and 1β (MIP-1β) were evaluated. Overall, glycemic levels increased, reached its maximum at 30 min (phase 1), returned to baseline levels at 120 min (phase 2), followed by a mild hypoglycemia at 180 min (phase 3). During phase 1, cytokine blood levels were maintained. However, we observed a synchronous fall (P<0.05) in the concentrations of pro-inflammatory (IL-15, IL-17, MCP-1) and anti-inflammatory cytokines (FGF-basic, IL-13, IL-1RA) during phase 2. Furthermore, a simultaneous rise (P<0.05) of pro-inflammatory (IL-2, IL-5, IL-17) and anti-inflammatory cytokines (IL-4, IL-1RA, IL-2R, IL-13, FGF-basic) occurred during phase 3. Thus, mild acute hypoglycemia but not a physiological increase of glycemia was associated with increased blood levels of anti-inflammatory and pro-inflammatory cytokines.
我们评估了在口服葡萄糖耐量试验期间,餐后血糖对非糖尿病且有反应性低血糖症状患者血液中促炎和抗炎细胞因子水平的影响。11例有反应性低血糖临床症状的患者口服葡萄糖溶液(75克)。在摄入葡萄糖后的0(基线)、30、60、120和180分钟采集血液,评估血浆中干扰素-α(IFN-α)、干扰素-γ(IFN-γ)、白细胞介素-1受体拮抗剂(IL-1RA)、白细胞介素2(IL-2)、白细胞介素-2受体(IL-2R)、白细胞介素4(IL-4)、白细胞介素6(IL-6)、白细胞介素8(IL-8)、白细胞介素10(IL-10)、白细胞介素-12(IL-12)、白细胞介素13(IL-13)、白细胞介素15(IL-15)、白细胞介素17(IL-17)、IFN-γ诱导蛋白10(IP-10)、单核细胞趋化蛋白1(MCP1)、IFN-γ诱导的单核因子(MIG)、巨噬细胞炎性蛋白-1α(MIP-1α)、白细胞介素-1β(IL-1β)、集落刺激因子(G-CSF)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)、碱性成纤维细胞生长因子(FGF-碱性)、嗜酸性粒细胞趋化因子、肿瘤坏死因子α(TNFα)、表皮生长因子(EGF)、肝细胞生长因子(HGF)、血管内皮生长因子(VEGF)、巨噬细胞炎性蛋白-1α(MIP-1α)和1β(MIP-1β)的浓度。总体而言,血糖水平升高,在30分钟时达到峰值(第1阶段),在120分钟时恢复到基线水平(第2阶段),随后在180分钟时出现轻度低血糖(第3阶段)。在第1阶段,细胞因子血液水平保持稳定。然而,我们观察到在第2阶段促炎细胞因子(IL-15、IL-17、MCP-1)和抗炎细胞因子(FGF-碱性、IL-13、IL-1RA)的浓度同步下降(P<0.05)。此外,在第3阶段促炎细胞因子(IL-又译为白细胞介素,下同)(IL-2、IL-5、IL-17)和抗炎细胞因子(IL-4、IL-1RA、IL-2R、IL-13、FGF-碱性)同时升高(P<0.05)。因此,轻度急性低血糖而非血糖的生理性升高与抗炎和促炎细胞因子血液水平升高有关。