糖耐量减低患者血清瘦素与内皮素-1 的测定及其临床意义

目的:探讨糖耐量减低(IGT)患者血清瘦素(Leptin)和血浆内皮素-1(ET-1)含量变化及其意义。方法:采用放射免疫法检测65例IGT患者、50名正常健康体检者和50例2型糖尿病患者血清中Leptin和ET-1的含量,同时分别测定体重指数、腰臀比、空腹血糖(FBG)、餐后2小时血糖(2h PBG)及空腹胰岛素(FINS),并用HOMA稳态模型计算胰岛素抵抗指数(HOMA-IR)。结果:糖尿病组、IGT组血清Leptin、ET-1、FBG、2hPBG、FINS、TC含量及HOMA-IR指数显著高于正常对照组(P<0.05),糖尿病组血清Leptin、ET-1、FBG、2hPBG、FINS、TC含量及HOMA-IR指数明显高于IGT组(P<0.05)。IGT组血清Leptin水平与BMI、血清ET-1、FBG、2hPBG、FINS、TC含量及HOMA-IR指数呈显著正相关(P<0.01),IGT组血清ET-1水平与收缩压、舒张压、BMI、血清FBG、2hPBG、FINS含量及HOMA-IR指数呈显著正相关(P<0.01)。结论:瘦素与内皮素-1均可能在IGT发展成2型糖尿病过程中起一定的作用。     

血清镁、血小板聚集率在糖耐量减低患者微血管病变中的临床意义

目的:观察糖耐量减低患者微血管病变与血清镁、血小板聚集率(PAR)的相关性。方法:将2012年11月-2014年1月在本院内分泌科和体检中心的120例研究对象随机均分为糖耐量减低合并微血管病变组(n=30),糖耐量减低无微血管病变组(n=30),糖尿病组(n=30),正常对照组(n=30)。比较各组患者的生化指标、血清镁与PAR的相关性、血镁水平以及PAR与FPG、HbA1C相关性。结果:糖尿病组和糖耐量减低合并微血管病变组患者的所有生化指标与对照组相比,差异有显著性(P0.05);血清镁水平与PAR之间呈显著负相关(P0.01);血镁水平与糖耐量减低合并微血管病变组、糖耐量减低无微血管病变组、糖尿病组中FPG、HbA1C呈负相关关系(P0.05);PAR与糖耐量减低合并微血管病变组、糖耐量减低无微血管病变组、糖尿病组中FPG、HbA1C呈正相关关系(P0.05)。结论:血清镁与PAR在预测糖耐量患者微血管病变中有一定的临床意义,值得临床推广。     

原发性高血压合并糖耐量减低患者窦性心率震荡分析

目的:观察单纯高血压痛(essential hypertension,EH)合并糖耐量减低(impaired glucose tolerance,IGT)患者窦性心率震荡(HRT)的变化,探讨其与自主神经功能损伤的关系.方法:45例EH及40例EH+IGT患者以及30例正常对照组入选,均接受24h动态心电图(DCG)记录,计算窦性HRT的初始值(TO)、震荡斜率值(TS),分析其与自主神经功能的关系.结果:原发性高血压患者有显著的HRT减弱,表现为TO升高、TS降低,其中合并IGT患者较普通高血压患者更加明显.结论:EH患者有显著的HRT减弱,其中EH合并IGT者较单纯的EH患者更加明显,证明心脏自主神经功能异常在EH,特别是EH并IGT患者中的重要作用.     

缺血性脑卒中患者血清C-反应蛋白和内皮素-1水平变化及临床意义

目的:探讨缺血性脑卒中患者不同病变时期血清C-反应蛋白(CRP)和内皮素-1(ET-1)水平变化与缺血性脑卒中关系.方法:临床确诊缺血性脑卒中患者68例,分别检测不同病变时期(入院时、入院第7天和出院前)的血清CRP和ET-1的含量,并记录病例的神经功能缺损评分.选择30例除外心脑血管疾病的体检者作为对照组.结果:①血清CRP含量在入院时、入院第7天和出院前分别为6.83±1.51 mg/L、4.89±1.33 mg/L、4.12±1.24 mg/L.较对照组(2.82±0.66 mg/L)均有显著升高(p＜0.05);血清ET-1含量在入院时、入院第7天和出院前分别为133.69±38.93 ng/L、125.234±32.45 ng/L、108.32±31.51 ng/L,较对照组(45.67±10.02mg/L)均有显著升高(p＜0.01).②随着病程的发展,CRP含量逐渐下降,与病程呈负相关,与神经功能缺损评分呈正相关;ET-1含量也逐渐下降,但仍维持在较高水平,与病程进展和神经功能缺损程度无明显的相关性.结论:缺血性脑卒中患者血清CRP和ET-1水平存在着动态变化.随着病情恢复,CRP含量明显下降,但ET-1含量仍维持在较高水平.     

海带多糖对高脂血症小鼠血清瘦素水平及瘦素受体表达的影响

本实验目的在于探讨海带多糖对实验性高脂血症小鼠瘦素及其受体水平的影响及其可能的机制。将健康雄性昆明小鼠80只,随机分为正常饲料组和高脂饲料组,后组以高脂饲料喂养建立高脂血症动物模型。将建模成功的小鼠随机均衡分为高脂模型组和海带多糖治疗组,后组以海带多糖灌胃干预。自动生化分析仪检测小鼠空腹血脂水平,ELISA测定血清瘦素(Leptin)含量,免疫组织化学法和Western blot检测下丘脑组织中瘦素受体(Lep-R,OBR)蛋白表达,RT-PCR检测OBR mRNA表达。结果示海带多糖治疗组小鼠血脂及血清Leptin水平较模型组显著降低(P0.05),下丘脑OBR mRNA及其蛋白表达水平较模型组显著升高(P0.05)。说明海带多糖可以通过提高下丘脑OBR的水平,改善瘦素抵抗,从而发挥降脂作用。     

妊娠高血压综合征患者血清瘦素水平变化及意义

目的探讨妊娠高血压综合征(妊高征)患者血清瘦素含量的变化及其在妊高征发病中的意义。方法采用放射免疫分析法(R IA)测定50例妊高征患者(HDP组,其中妊娠期高血压组12例,轻度子痫前期组20例,重度子痫前期组18例)、50例正常晚孕妇女(对照组)患者血清瘦素。结果 HDP组的血清瘦素值(24.23±7.94)μg/L显著高于对照组(10.12±3.15)μg/L(P<0.001),以子痫前期组增高明显。结论血清瘦素水平与妊高征的发生和病情程度有关。     

内皮素家系的新成员--内皮素1-31

内皮素1-31(endothelins1-31,ETs1-31)是糜酶水解内皮素原产生的一种成熟内皮素,有ET-11-31、ET-21-31和ET-31-31引三种异构体,目前已检测到ETs1-31分布于人、猴和仓鼠的粒细胞、肝脏、肺、气管、肾和肾上腺等组织。ETs1-31具有促细胞增殖、收缩平滑肌、升高平滑肌细胞游离Ca^2 、引起炎性细胞趋化和致心律失常等生物学效应,也可经内皮素转换酶水解为ETs1-21而间接产生效应。ETs1-31很可能与支气管哮喘、先兆子痫、动脉粥样硬化和肾小球肾炎等疾病密切相关。     

冠心病患者体内瘦素与高敏C反应蛋白检测的临床意义

目的:研究血清瘦素(LP)与高敏C反应蛋白(hsCRP)水平在冠心病患者体内的变化,及临床检测意义。方法:入选住院确诊的冠心病住院患者168例,对照组62例。外周血白细胞(WBC)水平应用全自动血细胞计数仪检测,血清高敏C反应蛋白水平应用比浊法检测,并血清瘦素水平用酶联免疫吸附法检测,分析瘦素与高敏C反应蛋白和外周血白细胞的关系。结果:(1)冠心病稳定型心绞痛组、不稳定型心绞痛组及急性心肌梗死组血清瘦素、高敏C反应蛋白和外周血白细胞水平显著高于对照组(均P0.05)。(2)血浆瘦素、高敏C反应蛋白及外周血白细胞水平在稳定型心绞痛组、不稳定型心绞痛组及急性心肌梗死组三组间依次增高,差异有统计学意义(均P0.05)。(3)简单相关分析显示瘦素与高敏C反应蛋白和外周血白细胞相关,r值分别为5.241和4.025,均P0.05。结论:瘦素与高敏C反应蛋白和外周血白细胞关系密切,可能通过炎症反应参与冠心病的发生。     

妊娠高血压综合征患者血清瘦素、TNF-α水平测定及其临床意义

目的检测妊娠高血压综合征患者血清中瘦素、TNF-α的水平,并探讨其与妊高征发病的关系。方法用放射免疫法测定35例妊高征患者外周血中瘦素及TNF-α的水平,并以21例正常晚期妊娠妇女(正常妊娠组)作比较。结果(1)妊高征组血清瘦素水平为(32.9±11.5)ng/ml,明显高于正常妊娠组的(18.9±3.0)ng/ml,P<0.05;轻度妊高征组血清瘦素水平为(22.0±4.8)ng/ml,与正常妊娠组比较,差异无显著性,P>0.05;中、重度妊高征组血清瘦素水平分别为(31.1±5.2)、(41.8±10.9)ng/ml,与轻度妊高征组及正常妊娠组比较,差异有显著性,P均<0.05;轻、中、重妊高征组之间血清瘦素水平差异有显著性(P均<0.05)。(2)妊高征组血清TNF-α水平为(22.7±11.5)fmol/ml,明显高于正常妊娠组的(9.2±2.1)fmol/ml,P<0.05,轻度妊高征组血清TNF-α水平为(11.5±4.1)fmol/ml,与正常妊娠组比较,差异无显著性,P>0.05;中、重度妊高征组血清TNF-α水平分别为(19.5±7.4)、(32.9±8.3)fmol/ml,与轻度妊高征组及正常妊娠组比较,差异有显著性(P均<0.05);轻、中、重妊高征组之间血清TNF-α水平差异有显著性(P均<0.05)。(3)妊高征组血清瘦素水平与TNF-α水平呈正相关(分别为r=0.56,P<0.01)。结论妊高征患者血清TNF-α水平增高可能是导致血清瘦素水平升高的原因之一。     

血清瘦素和胰岛素与犊牛初生重相关性

本实验旨在研究分娩奶牛(Bos taurus)、犊牛和脐静脉血瘦素、胰岛素之间的相关性及与犊牛初生重的相关性,为探究瘦素、胰岛素对犊牛初生重的影响机理提供理论数据。实验选取规模化养殖场正常分娩奶牛54头,按犊牛初生重划分为A组(≤40 kg)9头、B组(40~45 kg)25头、C组(≥45 kg)20头共3组,分别采集分娩奶牛、犊牛和脐静脉血,ELISA法检测血清瘦素、胰岛素含量。多组间采用单因素方差分析和双变量Pearson分析瘦素和胰岛素在各部位静脉血中表达的相关性及与犊牛初生重的相关性。结果表明:(1)奶牛静脉血瘦素、胰岛素含量极显著高于犊牛静脉血和脐静脉血(P0.01),奶牛静脉血瘦素、胰岛素含量与犊牛静脉血和脐静脉血瘦素、胰岛素相关性均不显著(P0.05);(2)瘦素、胰岛素含量在犊牛静脉血与脐静脉血之间均差异不显著(P0.05),犊牛静脉血瘦素、胰岛素含量与脐静脉血瘦素、胰岛素均分别呈极显著正相关(P0.01);(3)奶牛静脉血和脐静脉血中瘦素与胰岛素含量均呈显著正相关(P0.05),而犊牛静脉血中瘦素与胰岛素相关性不显著(P0.05);(4)犊牛初生重与奶牛静脉血瘦素、胰岛素含量均不相关(P0.05),但与犊牛静脉血和脐静脉血瘦素含量显著正相关(P0.05),与犊牛静脉血和脐静脉血胰岛素含量极显著正相关(P0.01);(5)奶牛静脉血、犊牛静脉血和脐静脉血瘦素和胰岛素含量在公犊牛与母犊牛间均无显著差异(P0.05)。可见,奶牛静脉血、犊牛静脉血和脐静脉血均有瘦素、胰岛素表达,且其含量奶牛静脉血显著高于犊牛静脉血和脐静脉血。奶牛静脉血瘦素、胰岛素含量与犊牛初生重相关性不显著,而犊牛静脉血和脐静脉血瘦素、胰岛素含量与犊牛初生重显著正相关性。     

A correlational study between serum asymmetric dimethylarginine level and impaired glucose tolerance patients associated with obesity

Asymmetric dimethylarginine (ADMA) plays a vital role in the regulation of insulin sensitivity and has been shown as a potential marker for various disease, including type 2 diabetes mellitus (DM2). However, the correlation between ADMA and impaired glucose tolerance (IGT) and obesity has not been studied. A total of 195 subjects were involved in our study. The characteristics of the subjects in the study cohort were measured and analyzed. We found that the serum ADMA and C-reactive protein levels were significantly increased in IGT and diabetic patients, whereas the levels of lipoprotein A and adiponectin were decreased, especially in diabetic patients with obesity. The serum ADMA level was positively correlated to a homeostatic model assessment for insulin resistance, and multivariate regression analysis further indicated that ADMA was an independent factor for DM patients with obesity. Our study expands the understanding of the complicated relationship between obesity, insulin resistance, IGT, and ADMA. In addition, we demonstrated that the serum ADMA level could serve as a diagnositic biomarker of the early signs for IGT patients with obesity.     

原发性高血压患者血浆ET-1含量与血小板参数相关性研究

目的:探讨血浆内皮素-1 (Endothelin-1,ET-1)含量变化和血小板功能异常在原发性高血压疾病进程中相关性及意义.方法:选择98例原发性高血压患者作为实验组和30例健康受试者作为正常对照组.实验组又根据高血压分级标准分为轻度高血压组(L组),中度高血压组(M组)和重度高血压组(S组),分别检测各组患者血浆ET-1含量和血小板各项参数值.结果:实验组血浆ET-1含量、平均血小板体积(mean platelet volume,MPV)、血小板分布宽度(platelet distribution width,PDW)明显高于对照组(P＜0.05),血小板计数(platelet count,PLT)和血小板压积(platelet hematocrit,PCT)明显低于对照组(P＜0.05);L组、M组和S组ET-1含量、MPV和PDW值呈进行性升高(P＜0.05),PLT和PCT值呈进行性降低(P＜0.05).结论:血浆ET-1含量和血小板各项参数变化与疾病的进展和危重程度存在相关性,对原发性高血压的诊断治疗及预后评估有重要意义.     

Ameliorating effect and potential mechanism of Rehmannia glutinosa oligosaccharides on the impaired glucose metabolism in chronic stress rats fed with high-fat diet

The aim of this study was to determine whether the Rehmannia glutinosa oligosaccharides (ROS) ameliorate the impaired glucose metabolism and the potential mechanism in chronic stress rats fed with high-fat diet. The rats were fed by a high-fat diet and simultaneously stimulated by chronic stress over 5 weeks. Body weight, fasting plasma glucose, intraperitoneal glucose tolerance test (IPGTT), plasma lipids, gluconeogenesis test (GGT), glycogen content, and corticosterone, insulin and leptin levels were measured. The results showed that ROS administration (100, 200 mg/kg, i.g.) for 5 weeks exerted the effects of increasing the organ weights of thymus and spleen, lowering the fasting plasma glucose level, improving impaired glucose tolerance, increasing the contents of liver and muscle glycogen, decreasing the gluconeogenesis ability, plasma-free fatty acid's level, as well as plasma triglyceride and total cholesterol levels in chronic stress and high-fat fed rats, especially in the group of 200 mg/kg; while the plasma corticosterone level was decreased, and plasma leptin level was increased. These results suggest that ROS exert an ameliorating effect of impaired glucose metabolism in chronic stress rats fed with high-fat diet, and the potential mechanism may be mediated through rebuilding the glucose homeostasis in the neuroendocrine immuno-modulation (NIM) network through multilinks and multitargets.     

ET-1与NT-proBNP浓度变化对高血压左心室肥厚的诊断价值

目的:探讨高血压左心室肥厚(Left ventricular hypertrophy,LVH)患者血浆内皮素(Endothelin,ET-1)、氨基末端脑钠肽前体(N-terminal pro brain natriuretic peptide,NT-proBNP)的浓度变化及其诊断价值。方法:收集2011年3月-2013年5月我医院确诊为高血压LVH患者128例设为观察组,选取同期128例体检正常人作为对照组。分析比较两组ET-1、NT-proBNP的浓度。结果:观察组血浆NT-proBNP及ET-1浓度分别为(6.4±3.5)pg/m L和(18.4±1.5)pg/m L,显著高于对照组,差异有统计学意义(P0.05);ROC图显示,NT-proBNP曲线下面积为0.932,可信区间为0.886-0.988,灵敏度为97.8%,特异度为79.9%;血浆ET-1曲线下面积为0.798,可信区间为0.709-0.892,灵敏度为65%,特异度为93.1%。结论:高血压LVH患者NT-proBNP及血浆ET-1水平显著高于正常人,对高血压LVH患者NT-proBNP及血浆ET-1的诊断具有重要意义。     

Occurrence of spontaneous diabetes mellitus in a cynomolgus monkey (Macaca fascicularis) and impaired glucose tolerance in its descendants

Spontaneous diabetes mellitus was diagnosed in a cynomolgus monkey. Clinical and pathological features, such as abnormal glucose tolerance, loss of insulin response, or degeneration of pancreatic beta-cells, resemble human noninsulin-dependent diabetes mellitus. Two descendants of the monkey have developed impaired glucose tolerance and insulin response. Genetic factors seem involved in the appearance of carbohydrate intolerance in this family group of monkeys.     

亚低温联合手术治疗对重型颅脑损伤患者血清ET-1、Ang-1、G-CSF及预后的影响

目的:研究亚低温联合手术治疗对重型颅脑损伤患者血清内皮素-1(endothelin-1,ET-1)、血管生成素-1(Angiopoietin-1,Ang-1)、粒细胞集落刺激因子(Granulocyte-colony stimulating factor,G-CSF)及预后的影响。方法:选取我院收治的118例重型颅脑损伤患者,按照抛硬币法分为治疗组和对照组,每组各59例。两组患者入院后均进行手术治疗,治疗组则在术后进行亚低温治疗。观察并比较两组患者临床治疗效果、治疗前后血清ET-1、Ang-1、G-CSF水平变化情况、不良反应发生情况以及预后情况。结果:治疗后,治疗组第1、3、7、14天的颅内压均显著低于对照组,两组组间比较差异显著(P0.05)。两组患者血清ET-1、Ang-1、G-CSF较治疗前显著下降,且治疗组血清各指标水平改善情况显著优于对照组(P0.05)。两组患者均发生脑梗死、脑积水、癫痫、肺部感染、切口脑脊液瘘以及应激性溃疡出血等并发症,但两组差异无统计学意义(P0.05)。治疗组患者的预后良好率达到49.15%,显著高于对照组的13.56%;而治疗组的死亡率(5.08%)则明显低于对照组(13.56%),两组差异显著(P0.05)。结论:亚低温联合手术治疗较单纯手术治疗可以更好的改善患者血清ET-1、Ang-1以及G-CSF水平,其不良反应发生率也更低,从而可以更好的改善患者的预后情况,值得在临床上推广应用。     

血浆FA、ET-1、Hcy、VEGF水平与妊娠高血压综合征的相关性研究

目的:研究叶酸(FA)、内皮素(ET-1)、同型半胱氨酸(Hcy)和血管内皮生长因子(VEGF)与妊娠高血压综合征的相关性。方法:选择2013年1月~2016年9月在我院进行诊治的妊娠高血压综合征患者80例,分为妊娠期高血压组即A组(40例)以及子痫前期、子痫组即B组(40例),60例正常晚期孕妇为C组,60例正常非孕妇为D组,分别检测各组的血浆FA、ET-1、Hcy和VEGF水平,并进行相关性分析。结果:四组间血浆FA、ET-1和Hcy水平相比,B组的血浆FA和VEGF水平最低(P0.05),ET-1和Hcy水平最高(P0.05);妊娠高血压综合征的妇女血浆FA和VEGF水平均低于正常晚期孕妇,ET-1和Hcy水平明显高于正常晚期孕妇(P0.05);多因素logistic回归分析显示FA、ET-1、Hcy、VEGF水平是妊娠高血压综合征的危险因素。结论:妊娠期FA缺乏引起血浆Hcy水平的升高可能与妊娠高血压综合征的发病及病情发展有关,VEGF可能是妊娠高血压综合征发生、发展的一个重要危险因素。     

Glucose intolerance in young TallyHo mice is induced by leptin-mediated inhibition of insulin secretion

The pathophysiology of TallyHo mouse, a recently established animal model for type 2 diabetes mellitus, was analyzed at prediabetic state to examine the inherent defects which contribute to the development of diabetes. At 4 weeks of age, the TallyHo mice already revealed glucose intolerance while their peripheral tissues exhibited normal insulin sensitivity. On the other hand, decreased plasma insulin concentration was observed with little differences in pancreatic insulin contents, indicating the impaired insulin secretion. Such defect, however, was not found in the isolated islets, which suggests a role of endocrine factor in impaired insulin secretion of TallyHo mice. Treatment of leptin inhibited the glucose-stimulated insulin secretion from the isolated islets of TallyHo mice, while in vivo administration of anti-leptin antibody lowered plasma glucose concentration with increased insulin level in TallyHo mice. Expression of glucokinase mRNA was decreased both in whole pancreas and leptin treated islets of TallyHo mice compared with whole pancreas in C57BL/6 mice and untreated islets of TallyHo mice, respectively. These results suggest that elevated plasma leptin can, through the inhibition of insulin secretion, induce glucose intolerance in TallyHo mice.     

Leptin deficiency impairs adipogenesis and browning response in mouse mesenchymal progenitors

Although phenotypically different, brown adipose tissue (BAT) and inguinal white adipose tissue (iWAT) are able to produce heat through non-shivering thermogenesis due to the presence of mitochondrial uncoupling protein 1 (UCP1). The appearance of thermogenically active beige adipocytes in iWAT is known as browning. Both brown and beige cells originate from mesenchymal stem cells (MSCs), and in culture conditions a browning response can be induced with hypothermia (i.e. 32 °C) during which nuclear leptin immunodetection was observed. The central role of leptin in regulating food intake and energy consumption is well recognised, but its importance in the browning process at the cellular level is unclear. Here, immunocytochemical analysis of MSC-derived adipocytes established nuclear localization of both leptin and leptin receptor suggesting an involvement of the leptin pathway in the browning response. In order to elucidate whether leptin modulates the expression of brown and beige adipocyte markers, BAT and iWAT samples from leptin-deficient (ob/ob) mice were analysed and exhibited reduced brown/beige marker expression compared to wild-type controls. When MSCs were isolated and differentiated into adipocytes, leptin deficiency was observed to induce a white phenotype, especially when incubated at 32 °C. These adaptations were accompanied with morphological signs of impaired adipogenic differentiation. Overall, our results indicate that leptin supports adipocyte browning and suggest a potential role for leptin in adipogenesis and browning.