2型糖尿病合并Hp感染者游离脂肪酸表达水平及氧化应激反应的变化研究
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摘要
目的观察2型糖尿病(type 2 diabetes mellitus, T2DM)合并幽门螺旋杆菌(helicobacter pylori,Hp)感染者血清游离脂肪酸(free fatty acid, FFA)及氧化应激反应的变化情况,探讨高血糖状态及Hp感染对血清FFA表达水平及氧化应激反应的影响。方法选取2017年1月至2018年6月利津县第二人民医院收治的160例T2DM患者(设为T2DM组)及50例健康体检者(设为对照组)作为研究对象,空腹采集肘部静脉血,检测血清FFA、丙二醛(malondialdehyde, MDA)的表达水平与超氧化物歧化酶(superoxide dismutase, SOD)的活性,以及Hp的感染情况。结果 T2DM组研究对象血清FFA、MDA表达水平明显高于对照组,SOD活性明显低于对照组,P均<0.01,差异具有统计学意义;对照组健康体检者均无Hp感染,T2DM组患者中存在Hp感染者69例,Hp感染率为43.1%; T2DM合并Hp感染者血清FFA、MDA表达水平明显高于非感染者,SOD活性明显低于非感染者,P均<0.01,差异具有统计学意义;T2DM合并Hp感染者血清FFA表达水平与MDA表达水平呈显著正相关、与SOD活性呈显著负相关。结论持续的高血糖状态及Hp感染均可提高T2DM患者体内FFA及MDA的表达水平,降低SOD的活性,增强患者体内的氧化应激反应,且以T2DM合并Hp感染者最为显著,而高浓度的FFA及高强度的氧化应激反应均可损伤胰岛β细胞的功能,进而引发胰岛素抵抗,加剧T2DM患者心、脑、肾等重要器官疾病的发生发展。
Objective To observe the changes of serum free fatty acids( FFA) and oxidative stress responses in patients with type 2 diabetes mellitus(T2 DM) complicated with helicobacter pylori(Hp) infection, and explore the effects of hyperglycemic state and Hp infection on Serum FFA expression and oxidative stress responses. Methods One hundred and sixty patients with T2 DM(T2 DM group) and fifty healthy persons underwent physical checkup(control group) in Lijin Second People's Hospital between January 2017 and June 2018 were selected as subjects. Elbow vein blood was collected on fasting to detect the expression levels of serum FFA and malondialdehyde( MDA), the activity of superoxide dismutase(SOD) and the condition of Hp infection. Results In the T2 DM group, the expression levels of FFA and MDA were obviously higher and the activity of SOD was markedly lower than that in the control group, and the differences were statistically significant, all P < 0. 01. No Hp infection was observed in the control group, while in the T2 DM group Hp infection was observed in 69 patients with the infection rate being 43. 1%. The expression levels of serum FFA and MDA in T2 DM patients with Hp infection were significantly higher and their SOD activity was obviously lower than that in the Hp-free T2 DM patients,and the differences were statistically significant, all P < 0. 01. In T2 DM patients complicated with Hp infection, the expression of serum FFA is significantly and positively associated with the expression of MDA while has a notably negative correlation with SOD activity. Conclusion Sustained hyperglycemic state and Hp infection can increase the expression of serum FFA and MDA, decrease the activity of SOD, and enhance the oxidative stress responses in T2 DM patients, especially in T2 Dm patients complicated with Hp infection. Moreover, the high concentration of FFA and high intensity of oxidative stress responses will damage the function of pancreatic β-cells and further induce the insulin resistance, exacerbating the development and progress of major organ diseases including heart, brain, kidneys and etc. in T2 DM patients.
Objective To observe the changes of serum free fatty acids( FFA) and oxidative stress responses in patients with type 2 diabetes mellitus(T2 DM) complicated with helicobacter pylori(Hp) infection, and explore the effects of hyperglycemic state and Hp infection on Serum FFA expression and oxidative stress responses. Methods One hundred and sixty patients with T2 DM(T2 DM group) and fifty healthy persons underwent physical checkup(control group) in Lijin Second People's Hospital between January 2017 and June 2018 were selected as subjects. Elbow vein blood was collected on fasting to detect the expression levels of serum FFA and malondialdehyde( MDA), the activity of superoxide dismutase(SOD) and the condition of Hp infection. Results In the T2 DM group, the expression levels of FFA and MDA were obviously higher and the activity of SOD was markedly lower than that in the control group, and the differences were statistically significant, all P < 0. 01. No Hp infection was observed in the control group, while in the T2 DM group Hp infection was observed in 69 patients with the infection rate being 43. 1%. The expression levels of serum FFA and MDA in T2 DM patients with Hp infection were significantly higher and their SOD activity was obviously lower than that in the Hp-free T2 DM patients,and the differences were statistically significant, all P < 0. 01. In T2 DM patients complicated with Hp infection, the expression of serum FFA is significantly and positively associated with the expression of MDA while has a notably negative correlation with SOD activity. Conclusion Sustained hyperglycemic state and Hp infection can increase the expression of serum FFA and MDA, decrease the activity of SOD, and enhance the oxidative stress responses in T2 DM patients, especially in T2 Dm patients complicated with Hp infection. Moreover, the high concentration of FFA and high intensity of oxidative stress responses will damage the function of pancreatic β-cells and further induce the insulin resistance, exacerbating the development and progress of major organ diseases including heart, brain, kidneys and etc. in T2 DM patients.
引文
[1]陈凯,卢乐,蔡恩照,等.2型糖尿病患者幽门螺杆菌感染与胰岛素抵抗的关系[J].中国慢性病预防与控制,2016, 24(11):851-853.
[2]安振国,杨文东.2型糖尿病合并冠心病与幽门螺杆菌感染的相关性研究[J].国际医药卫生导报,2014, 20(18):2872-2875.
[3]杨文东.原发性高血压患者颈动脉粥样硬化与幽门螺杆菌感染的相关性研究[J].中国医师杂志,2014, 16(3):347-349, 352.
[4]杨文东.游离脂肪酸与妊娠期糖尿病胰岛素抵抗的关系[J].现代检验医学杂志,2013, 28(1):124-126.
[5]许银银,刘北忠.血清游离脂肪酸、同型半胱氨酸与代谢综合征的相关性研究[J].检验医学与临床,2015, 12(21):3131-3132, 3136.
[6]赵佳,左林,姚创利,等.冠心病患者血清同型半胱氨酸水平与氧化应激的关系研究[J].现代检验医学杂志,2016, 31(5):27-29.
[7]中华医学会糖尿病学分会.中国2型糖尿病防治指南(2013年版)[J].中华糖尿病杂志,2014, 6(7):447-498.
[8]杜洁,杨维,张桂侠,等.幽门螺杆菌感染与血脂代谢及动脉粥样硬化的相关性[J].现代检验医学杂志,2017, 32(4):104-106.
[9]杜洁,朱娜,李红艳,等.幽门螺杆菌感染对慢性阻塞性肺疾病血气分析及肺功能的影响[J].现代检验医学杂志,2017,32(6):99-101.
[10]崔卫东.空腹血清游离脂肪酸与2型糖尿病的相关性分析[J].检验医学,2013, 28(7):637-639.
[11]王依屹,张珏,鲁传翠.2型糖尿病患者胰岛素抵抗与血清游离脂肪酸浓度的关系[J].检验医学,2012, 27(10):806-808.
[12] Hakim FA, Pflueger A. Role of oxidative stress in diabetic kidney disease[J]. Med Sci Monit, 2010, 16(2):37-48.
[13]刘蕊,戴岳.糖尿病肾病发病机制的研究进展[J].药学与临床研究,2018, 26(3):202-205.
[14]朱文奎,徐绮,陈晋.血清钙、游离脂肪酸与社区老年代谢综合征的相关性分析[J].检验医学,2018, 33(5):407-410.
[15]陈效琴,任静.游离脂肪酸、胰岛素抵抗与代谢综合征相关因素的关系[J].检验医学,2016, 31(7):553-558.
[16] Saxena R, Kaur J. Thl/Th2 cytokines and their genotypes as predictors of hepatitis B virus related hepatocellular carcinoma[J].World J Hepatol, 2015, 7(11):1572-1580.
[17] Verit A, Yuksel OH, Kivrak M, et al. Are helicobacter pylori and benign prostatic hyperplasia related, and if so, how?[J].Urol J, 2015,12(4):2271-2275.
[18]郝志华,陈春彦,王俊明,等.糖尿病患者幽门螺杆菌感染情况及颈动脉粥样硬化相关因素研究[J].中国全科医学,2012, 15(17):1914-1916.
[19]张同庆,杨文东.急性脑梗死并发幽门螺旋杆菌感染者血脂水平及氧化应激反应的观察[J].现代检验医学杂志,2018, 33(2):66-69.
[20]胡彩虹,韦锦涛,郭东亮.游离脂肪酸检测在2型糖尿病胰岛素抵抗临床应用[J].糖尿病新世界,2017, 20(4):61-62.
[2]安振国,杨文东.2型糖尿病合并冠心病与幽门螺杆菌感染的相关性研究[J].国际医药卫生导报,2014, 20(18):2872-2875.
[3]杨文东.原发性高血压患者颈动脉粥样硬化与幽门螺杆菌感染的相关性研究[J].中国医师杂志,2014, 16(3):347-349, 352.
[4]杨文东.游离脂肪酸与妊娠期糖尿病胰岛素抵抗的关系[J].现代检验医学杂志,2013, 28(1):124-126.
[5]许银银,刘北忠.血清游离脂肪酸、同型半胱氨酸与代谢综合征的相关性研究[J].检验医学与临床,2015, 12(21):3131-3132, 3136.
[6]赵佳,左林,姚创利,等.冠心病患者血清同型半胱氨酸水平与氧化应激的关系研究[J].现代检验医学杂志,2016, 31(5):27-29.
[7]中华医学会糖尿病学分会.中国2型糖尿病防治指南(2013年版)[J].中华糖尿病杂志,2014, 6(7):447-498.
[8]杜洁,杨维,张桂侠,等.幽门螺杆菌感染与血脂代谢及动脉粥样硬化的相关性[J].现代检验医学杂志,2017, 32(4):104-106.
[9]杜洁,朱娜,李红艳,等.幽门螺杆菌感染对慢性阻塞性肺疾病血气分析及肺功能的影响[J].现代检验医学杂志,2017,32(6):99-101.
[10]崔卫东.空腹血清游离脂肪酸与2型糖尿病的相关性分析[J].检验医学,2013, 28(7):637-639.
[11]王依屹,张珏,鲁传翠.2型糖尿病患者胰岛素抵抗与血清游离脂肪酸浓度的关系[J].检验医学,2012, 27(10):806-808.
[12] Hakim FA, Pflueger A. Role of oxidative stress in diabetic kidney disease[J]. Med Sci Monit, 2010, 16(2):37-48.
[13]刘蕊,戴岳.糖尿病肾病发病机制的研究进展[J].药学与临床研究,2018, 26(3):202-205.
[14]朱文奎,徐绮,陈晋.血清钙、游离脂肪酸与社区老年代谢综合征的相关性分析[J].检验医学,2018, 33(5):407-410.
[15]陈效琴,任静.游离脂肪酸、胰岛素抵抗与代谢综合征相关因素的关系[J].检验医学,2016, 31(7):553-558.
[16] Saxena R, Kaur J. Thl/Th2 cytokines and their genotypes as predictors of hepatitis B virus related hepatocellular carcinoma[J].World J Hepatol, 2015, 7(11):1572-1580.
[17] Verit A, Yuksel OH, Kivrak M, et al. Are helicobacter pylori and benign prostatic hyperplasia related, and if so, how?[J].Urol J, 2015,12(4):2271-2275.
[18]郝志华,陈春彦,王俊明,等.糖尿病患者幽门螺杆菌感染情况及颈动脉粥样硬化相关因素研究[J].中国全科医学,2012, 15(17):1914-1916.
[19]张同庆,杨文东.急性脑梗死并发幽门螺旋杆菌感染者血脂水平及氧化应激反应的观察[J].现代检验医学杂志,2018, 33(2):66-69.
[20]胡彩虹,韦锦涛,郭东亮.游离脂肪酸检测在2型糖尿病胰岛素抵抗临床应用[J].糖尿病新世界,2017, 20(4):61-62.