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目的:研究谷氨酸脱羧酶抗体(GAD-Ab)与Graves'病病程及浸润性突眼的关系。方法:用ELISA法测定51例Graves'病患者血清中的GAD-Ab。结果:20例阳性,阳性率39.2%,其中病程<6月组,GAD-Ab阳性率7.7%,明显低于病程>6月组(P<0.01),Graves′病并浸润性突眼组,阳性率为57.7%,明显高于非浸润性突眼组(P<0.01)。结论:GAD-Ab的测定有助于了解Graves'病病程及监测浸润性突眼。 相似文献
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核因子κB(NF-κB)通过促进细胞因子、活性氧簇和Fas相关基因的表达介导的β细胞凋亡,可以诱发1型糖尿病.阻断依赖NF-κB的信号通路,对抗β细胞凋亡,能为糖尿病(特别是1型糖尿病)的防治提供新的手段. 相似文献
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核因子κB(NF-κB)通过促进细胞因子、活性氧簇和Fas相关基因的表达介导的β细胞凋亡,可以诱发1型糖尿病。阻断依赖NF-κB的信号通路,对抗β细胞凋亡,能为糖尿病(特别是1型糖尿病)的防治提供新的手段。 相似文献
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葛根素对去卵巢大鼠骨密度和骨代谢生化指标的影响 总被引:1,自引:0,他引:1
目的:研究葛根素对去卵巢大鼠骨密度和骨代谢生化指标的影响,探讨葛根素对雌激素缺乏引起的骨质疏松的治疗作用。方法:3月龄SD大鼠32只,随机分为单纯卵巢摘除组,假手术组,雌激素治疗组和葛根素治疗组,手术后7d,雌激素组给予苯甲酸雌二醇,200μg/kg皮下注射,每周两次;葛根素组给予葛根素注射液50mg/kgl皮下注射,1次/d;单纯卵巢摘除组与假手术组每日皮下注射与葛根素组和雌激素组同等体积的生理盐水,10周后测量大鼠骨密度、子宫系数、血尿中骨代谢生化指标。结果:与单纯卵巢摘除组相比,葛根素组大鼠骨密度(g/cm2)明显升高(0.112±0.002和0.106±0.004,t=-3.851,P<0.05),血碱性磷酸酶犤(1.26±0.14)和(2.14±0.63)mkat犦、尿钙/尿肌酐(0.209±0.069和0.237±0.050)、尿脱氧吡啶啉/尿肌酐下降(6.517±1.374和9.592±3.507),差异有显著性意义(t=3.858,-3.823,2.309,P均<0.05),血雌二醇升高犤(6.188±4.350)和(3.385±3.811)ng/L,t=3.858P<0.05犦;与雌二醇组相比,葛根素组子宫系数(g/kg)明显降低,差异有显著性意义(1.053±0.735和4.265±1.446,t=5.610,P<0.01)。结论:葛根素具有与雌激素类似的减少骨吸收,促骨形成,增加骨密度的作用,而在刺激子宫组织增生的副作用方面又远较雌激素为轻。 相似文献
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目的 研究血管紧张素Ⅱ受体拮抗剂(ARB)氯沙坦对2型糖尿病、糖尿病肾病患者微量白蛋白尿的治疗效果.方法 血压正常的2型糖尿病患者43例,其尿白蛋白排泄率(UAER)在20~200 μg/min之间,其血糖控制在可接受水平[空腹血糖(FBG)≤7 mmol/L,餐后2 h血糖(P2hBG)≤10 mmol/L].随机分为治疗组23例,对照组20例,对照组在控制血糖基础上加用安慰剂,治疗组加用ARB氯沙坦50 mg/d.两组患者在治疗前和治疗12周后复查FBG、P2hBG、糖化血红蛋白(HbA1c)和UAER.结果 治疗12周后,治疗组UAER为(76±11)μg/min,与治疗前(119±14)μg/min相比明显下降(P<0.05),与对照组(125±13)μg/min比较,差异有显著性(P<0.05).结论 对血压正常的2型糖尿病早期糖尿病肾病患者,ARB氯沙坦在对血压无影响的情况下具有独特的降低尿微量白蛋白水平,延缓糖尿病肾病进展的作用. 相似文献
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Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis. 相似文献
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吸烟对2型糖尿病患者血清细胞黏附分子水平和氧化应激的影响 总被引:1,自引:0,他引:1
目的 探讨吸烟对男性2型糖尿病(T2DM)患者血清细胞黏附分子(CAM)水平和氧化应激的影响.方法 选择112例男性T2DM患者,其中吸烟T2DM患者63例,非吸烟T2DM患者49例,另选择30例男性非吸烟健康者为对照组.检测3组受检者血清可溶性细胞间黏附分子-1(sICAM-1)、可溶性血管细胞黏附分子-1(sVCAM-1)、E-选择素、丙二醛水平及超氧化物歧化酶(SOD)活性.结果 吸烟T2DM组患者血清丙二醛、sICAM-1、sVCAM-1水平及SOD活性[分别为(8.2±3.6)、(1 033±201)μg/L、(2.2±1.5)μg/L、(71±10)U/ml]与对照组[分别为(4.2±2.4)μmol/L、(579±112)μg/L、(1.4±0.9)μg/L和(105±16)U/ml]及非吸烟T2DM组[分别为(6.5±4.9)μmol/L、(899±121)μg/L、(1.4±0.8)μg/L和(82±11)U/ml]比较,差异均有统计学意义(P<0.05).吸烟T2DM患者和非吸烟T2DM患者E-选择素水平[(62±28)μg/L和(59±19)μg/L]与对照组[(41±15)μg/L]比较,差异均有统计学意义(P<0.05).重度吸烟T2DM组患者血清sICAM-1、丙二醛水平[分别为(1 119±188)μg/L、(9.5±3.4)μmol/L]及SOD活性[(61±10)U/ml]与非吸烟T2DM组[分别为(899±121)μg/L、(6.5±4.9)μmol/L和(82±11)U/ml]、轻度吸烟T2DM组[分别为(938±137)μg/L、(7.6±2.4)μmol/L和(77±9)U/ml]、中度吸烟T2DM组[分别为(986±151)μg/L、(8.3±2.5)μmol/L和(67±12)U/ml]比较,差异均有统计学意义(P<0.05);中度吸烟T2DM组患者血清sICAM-1、丙二醛水平及SOD活性与非吸烟T2DM组、轻度吸烟T2DM组比较,差异亦均有统计学意义(P<0.05).吸烟T2DM患者血清sICAM-1水平与收缩压、胰岛素抵抗指数(HOMA-IR)及丙二醛、E-选择素水平呈正相关(r值分别为0.36、0.29、0.38、0.28,P<0.05),与SOD活性呈负相关(r=-0.25,P<0.05);血清sVCAM-1水平与收缩压、HOMA-IR、丙二醛水平呈正相关(r值分别为0.25、0.28、0.32,P<0.05);E-选择素水平与HOMA-IR、sICAM-1、丙二醛水平呈正相关(r值分别为0.31、0.28、0.30,P<0.05),与SOD活性呈负相关(r=-0.22,P<0.05).结论 吸烟可增加男性T2DM患者血清CAM水平及氧化应激,且吸烟量与sICAM-1和氧化应激水平相关. 相似文献
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糖尿病肺病变 总被引:36,自引:0,他引:36
沈兴平 《重庆医科大学学报》1997,22(3):270-271
糖尿病肺病变临床学院内分泌科沈兴平,综述舒昌达审校中图分类号R587.2糖尿病(DM)慢性并发症的主要发病机制是微血管病变和组织蛋白质非酶糖基化(NEG)[1]。DM长期高血糖,增加了肺组织蛋白质NEG,从而导致肺损害,本文拟就肺的形态、生化、肺功能... 相似文献