CAJ | 학술논문

目的探讨不同胰岛素敏感性个体炎症因子血浆水平以及炎症通路激活状态的差异.方法收集体检女性38例,按体重指数分为两组:肥胖组22例,正常对照组16名,稳态模型评估的胰岛素抵抗指数(HOMA-IR)评估研究对象胰岛素敏感性,检测炎症因子白细胞介素6(IL-6)、IL-1β血浆水平,Western印迹法检测外周血白细胞IκB激酶(IKK)、NFκB抑制物(IκB)及其磷酸化水平,以凝胶电泳迁移率分析(EMSA)评价核因子NFκB的结合活性.结果肥胖组空腹胰岛素[62.2(20.0～127.0)pmol/L对19.15(14.2～47.8)pmol/L,P<0.01]、HOMA-IR[2.32(0.76～5.49)对0.70(0.53～1.7),P<0.01]、HbAIC[(5.42±0.45)%对(5.08±0.38)%,P<0.05]、血甘油三酯[(1.75±0.68对1.22±0.58)mmol/L,P<0.05]、IL-6[3.15(0.03～22.2)pg/ml对1.26(0.74～6.06)pg/ml,P<0.01]和IL-1β[6.53(0.84～36)pg/ml对3.16(1.48-8.86)pg/ml,P<0.01]水平显著高于正常对照组,伴随外周血白细胞胞浆蛋白IKKα、IKKβ表达和IκBα丝氨酸磷酸化水平增高,IκBα表达下调,肥胖组NFκB结合活性较正常对照组显著增加.结论肥胖组炎症因子IL-6、IL-Iβ血浆水平显著升高.IKK-IκB-NFκB通路的激活与肥胖个体胰岛素抵抗的发生有关.
목적 탐토불동이도소민감성개체염증인자혈장수평이급염증통로격활상태적차이.방법 수집체검녀성38례,안체중지수분위량조:비반조22례,정상대조조16명,은태모형평고적이도소저항지수(HOMA-IR)평고연구대상이도소민감성,검측염증인자백세포개소6(IL-6)、IL-1β혈장수평,Western인적법검측외주혈백세포IκB격매(IKK)、NFκB억제물(IκB)급기린산화수평,이응효전영천이솔분석(EMSA)평개핵인자NFκB적결합활성.결과 비반조공복이도소[62.2(20.0～127.0)pmol/L대19.15(14.2～47.8)pmol/L,P<0.01]、HOMA-IR[2.32(0.76～5.49)대0.70(0.53～1.7),P<0.01]、HbAIC[(5.42±0.45)%대(5.08±0.38)%,P<0.05]、혈감유삼지[(1.75±0.68대1.22±0.58)mmol/L,P<0.05]、IL-6[3.15(0.03～22.2)pg/ml대1.26(0.74～6.06)pg/ml,P<0.01]화IL-1β[6.53(0.84～36)pg/ml대3.16(1.48-8.86)pg/ml,P<0.01]수평현저고우정상대조조,반수외주혈백세포포장단백IKKα、IKKβ표체화IκBα사안산린산화수평증고,IκBα표체하조,비반조NFκB결합활성교정상대조조현저증가.결론 비반조염증인자IL-6、IL-Iβ혈장수평현저승고.IKK-IκB-NFκB통로적격활여비반개체이도소저항적발생유관.
Objective To explore the difference involved in the activation of inflammation pathway and the plasma level of inflammatory factors in the subjects with different sorts of insulin sensitivity. Methods The study was carried out in 38 women, consisting of obesity (n = 22 ) and control (n = 16 ) groups according to body mass index. The insulin sensitivity was assessed by homeostasis model assessment of insulin resistance (HOMAIR). Plasma concentrations of interleukin-6 (II-6) and IL-1β were determined by enzyme immunoassay. Western blot analysis was used to examine total protein expression and phosphorylation levels of IκB kinase (IKK) ,inhibitor of nuclear factor-κB ( IκB ) in peripheral blood leukcocytes. Electrophoretic mobility shift assay (EMSA)was used to detect the binding activity of NFκB. Results The levels of fasting plasma insulin[62.2 ( 20.0-127. 0) pmol/L vs 19. 15 ( 14. 2-47. 8 ) pmol/L, P<0. 01], HOMA-IR[2. 32 ( 0. 76-5.49 ) vs 0.70(0.53-1.7),P<0.0l], HbA1 C[(5.42±0. 45 ) % vs ( 5.08 ±0. 38) %, P<0. 05], triglyceride[( 1.75 ±0. 68 vs 1.22 ±0. 58 )mmol/L, P<0. 05], plasma IL-6[3. 15 (0. 03-22. 2) pg/ml vs 1.26 (0. 74-6.06 ) pg/ml, P<0. 01], and IL-1 β[6. 53 ( 0. 84-36 ) pg/ml vs 3. 16( 1.48-8. 86 ) pg/ml, P<0. 01]in obesity group were significantly higher than those in control group. Compared with control group, the levels of IKKo, IKKβ expression and IκBα serine phosphorylation in obesity group were markedly increased, while the expression of IκBα was significantly reduced. Accompanied with the degradation of IκBα protein, the binding activity of NFκB in obesity group was significantly increased. Conclusions The plasma levels of IL-6 and IL-1β were significantly raised in obesity group. The activation of IKK-IκB-NFκB pathway is closely associated with the genesis and development of insulin resistance in obese subjects.