NIDDM患者中性粒细胞膜流动性的改变及其影响因素

目的检测６５例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者中性粒细胞（ＰＭＮ）膜流动性（ＭＦ）的改变,探讨这种改变与年龄、病程、ＢＭＩ、ＦＢＧ、ＰＢＧ、ＴＧ、ＴＣ、ＷＢＣ、ＲＢＣ、ＰＬＴ、ＧＰＩ的相关关系。方法６５例无酮症及感染的ＮＩＤＤＭ患者,３０例性别、年龄、ＢＭＩ相匹配的正常人为对照,以ＤＰＨ为探针测定其ＰＭＮ的荧光偏振值（ρ）,并计算相应的细胞膜流动性、膜脂各向异性及微粘度,对ＰＭＮ ρ值的影响因素进行分析。结果１ＮＩＤＤＭ患者的ＰＭＮｐ值显著高于对照组（Ｐ＜０．０１）,ＰＭＮ　ＭＦ明显低于对照组（Ｐ<０．０５）,ＰＭＮ膜脂各向异性及微粘度均显著升高（Ｐ<０．０１）。 ２ ＰＭＮ ＭＦ与ＦＢＧ、ＰＢＧ呈负相关（ｒ＝－０．３４１７,ｒ＝－０．３２３７,Ｐ<０．０５）,与ＧＰＩ相关性显著（ｒ＝－０．３９１３,Ｐ<０．０５）,与年龄、病程、ＢＭＩ、ＷＢＣ、ＲＢＣ、ＰＬＴ、ＴＧ、ＴＣ无相无性。结论ＮＩＤＤＭ患者ＰＭＮ的ＭＦ下降,显示ＤＭ患者ＰＭＮ膜的物理性质有明显改变;ＰＭＮ ＭＦ下降与血糖升高、血清蛋白糖化程度增加有关。     

非胰岛素依赖型糖尿病人血浆内皮素水平与游离脂肪酸浓度的关系

为探讨非胰岛素依赖型糖尿病（Ｎｏｎｉｎｓｕｌｉｎ－ｄｅｐｅｎｄｅｎｔｄｉａｂｅｔｅｓｍｅｌｌｉｔｕｓ,ＮＩＤＤＭ）人内皮细胞损伤的可能机制,作者采用放射免疫法和反相高效液相色谱技术（ＨＰＬＣ）同时测定了３４例正常人和５６例ＮＩＤＤＭ病人血浆内皮素（ＥＴ）和游离脂肪酸（ＦＦＡ）浓度。结果显示：ＮＩＤＤＭ病人血浆ＥＴ和ＦＦＡ浓度较正常对照明显升高（均ｐ＜０．０１）,且血浆ＥＴ与空腹血糖（ＦＢＧ）水平和ＦＦＡ总浓度呈明显正相关（ｒ＝０．３２４和,ｒ＝０．３５１,均Ｐ＜０．０１）。结果提示：ＮＩＤＤＭ患者高血糖、脂肪酸代谢紊乱及胰岛素抵抗在其血管内皮损伤中可能有重要作用。     

老年糖尿病人胰岛A,B细胞功能与血脂变化

对１９９２年１月～１９９４年１月收治的老年糖尿病２１０例，作者观察了胰岛Ａ、Ｂ细胞功能与血脂及血粘度的变化。老年ＮＩＤＤＭ的口服葡萄糖耐量试验各时相血糖值均显著增高（Ｐ＜０．０１）；胰岛素释放试验及Ｃ肽释放试验中，除空腹胰岛素及Ｃ肽值正常外，其余各时相值均明显降低，但其中有２０例呈高胰岛素血症（９．５％）；胰高糖素释放试验中，空腹与１８０分钟的胰高糖素值正常，其余各时相值均明显升高（Ｐ＜０．０１）。老年ＮＩＤＤＭ的ＧＨｂＡ＿（１ｃ）及ＧＨｂＡ＿１值显著增高（Ｐ＜０．０１），血胆固醇，甘油三脂，低密度脂蛋白，极低密度脂蛋白和全血粘度平均值均显著增高（Ｐ＜０．０１）．而高密度脂蛋白及血浆粘度等无明显变化。老年ＮＩＤＤＭ胰岛Ａ、Ｂ细胞功能失调，并经常有高血脂及高粘血症，少数有高胰岛素血症，容易并发心、脑、肾、眼或足的并发症，因此治疗老年糖尿病时，还应加强治疗高血脂症及高粘血症，以减少致残或死亡。     

扩张型心肌病可溶性IL－2R、NK活性和T细胞亚群的检测

应用单克隆与多克隆双抗体夹心法检测２０例扩张型心肌病（ＤＣＭ）及２０例正常人（ＮＣ）的血清可溶性白细胞介素２受体（ｓＩＬ－２Ｒ），同时测定了外周血自然杀伤细胞（ＮＫ）活性和Ｔ淋巴细胞亚群，结果发现ＤＣＭ患者ｓＩＬ－２Ｒ明显高于ＮＣ组（Ｐ＜０．００１），而ＮＫ活性明显低于ＮＣ组（Ｐ＜０．００１），ＤＣＭ患者Ｔ细胞亚群与ＮＣ组比较，ＣＤ８降低（Ｐ＜０．０１），而ＣＤ４／ＣＤ８比值升高（Ｐ＜０．０５）。提示细胞免疫功能紊乱参与ＤＣＭ的病理过程。     

扩张型心肌病细胞免疫的初步研究

本文应用免疫酶标染色法及微量细胞毒试验分别检测了扩张型心肌病（ＤＣＭ）外周血Ｔ淋巴细胞亚群ＣＤ３、ＣＤ４及ＣＤ８及自然杀伤细胞活性（ＮＫ），并与正常对照组（ＮＣ）比较，结果发现ＤＣＭ患者的ＣＤ８明显低于ＮＣ组（Ｐ〈０．０１），而ＣＤ４／ＣＤ８比值高于ＮＣ组（Ｐ〈０．０５）；同时发现ＮＫ活性低于ＮＣ组（Ｐ〈０．００１）。因此推测Ｔ淋巴细胞亚群异常及ＮＫ活性缺失所致的细胞免疫功能紊乱可能是ＤＣＭ发病的     

糖尿病患者红细胞钙含量与红细胞变形性

用火焰原子吸收法测定Ⅱ型糖尿病（ＮＩＤＤＭ）２４例红细胞钙总量及用激光衍射法测定其红细胞变形性（ＲＣＤ）。测定５０例ＮＩＤＤＭ之红细胞在１５０、２００、２５０、３００及３５０ｍｍｏｌ／Ｌ５种渗透压悬液中的变形性。结果表明，正常成人红细胞钙总量为３３．６２±１２．８０μｍｏｌ／Ｌ，ＲＣＤ降低的ＮＩＤＤＭ患者，其红细胞钙总量明显升高（４６．３７±２３．３７μｍｏｌ／Ｌ，Ｐ＜０．０５），而ＲＣＤ正常之患者则接近正常水平。不同渗透压悬液中的最大ＤＩ值（ＤＩｍａｘ）显示，ＲＣＤ降低之ＮＩＤＤＭ红细胞在２５０及３００ｍｍｏｌ／Ｌ的ＤＩｍａｘ显著减小（Ｐ＜０．００１）；而在１５０及２００ｍｍｏｌ／Ｌ的低渗范围，其ＤＩｍａｘ接近正常，符合内粘度加大的ＤＩｍａｘ渗透压曲线特征。     

糖尿病肾病患者24小时尿Alb,β2—MG,THP,C—肽RIA测定的？…

用放射免疫分析（ＲＩＡ）测定了５３例糖尿病和３４例糖尿病肾病（ＤＮ）患者２４小时尿白蛋白（Ａｌｂ）、β２微球蛋白（β２－ＭＧ）、Ｔａｍｍ－Ｈｏｒｓｆａｌｌ蛋白（ＴＨＰ）、Ｃ－肽的排泄量并分析其相互间比值的变化，以探讨肾脏病变化发生的部位及病损程度。结果发现：糖尿病组与糠尿病肾病组比较，差异非常显著（Ｐ〈０．００１）；糠尿病组Ａｌｂ与β２－ＭＧ呈正相关ｒ１＝０．３１４（Ｐ〈０．０５）与ＴＨＰ、Ｃ－肽     

非小细胞肺癌患者放疗前后机体免疫功能变化的研究

目的：报道３０例非小细胞肺癌（ＮＳＣＬＣ）患者放疗前后免疫功能的变化。方法：采用双抗体夹心法和比浊法检测血清中ｓＩＬ－２Ｒ、免疫球蛋白（ＩｇＧ,ＩｇＡ,ＩｇＭ）含量,用单克隆抗体和流式细胞仪技术检测外周血中Ｔ细胞亚群,Ｂ细胞,ＮＫ细胞百分数;与健康人做对照。结果：放疗前ｓＩＬ－２Ｒ显著增高（Ｐ〈０．０１）,ＩｇＧ及ＩｇＭ６亦增高（Ｐ〈０．０５）,Ｂ细胞百分数低于（Ｐ〈０．０１）,ＣＤ３＾＋细胞降低     

rIL—2逆转扩张型心肌病NK细胞活性的研究

本文检测了扩张型心肌病（ＤＣＭ）、冠心病（ＣＨＤ）和正常人（ＮＣ）的自然杀伤细胞（ＮＫ）数目及活性。结果发现ＤＣＭ患者ＮＫ数目与ＣＨＤ及ＮＣ组比较无统计学差异（Ｐ＞０．０５），而ＮＫ活性低于其它二组（Ｐ＜０．００１）。经重组白细胞介素２（ｒＩＬ－２）温育ＮＫ后，ＮＫ活性明显升高（Ｐ＜０．００１），同时ＮＫ活性与ＤＣＭ病情严重程度有关，提示ＮＫ和ＤＣＭ发病中有意义，并可作为判断ＤＣＭ病情严重程度的指     

扩张型心肌病可溶性IL—2R,NK活性和T细胞亚群的检测

应用单克隆与多克隆双抗体夹心法检测２０例扩张型心肌病及２０例正常人的血清可溶性白细胞介素２受体，同时测定了外周血自然余伤细胞活性和Ｔ淋巴细胞亚群，结果发现，ＤＣＭ患者ｓＩＬ－２Ｒ明显高于ＮＣ组（Ｐ＜０．００１），而ＮＫ活性明显低于ＮＣ组（Ｐ＜０．００１），ＤＣＭ患者Ｔ细胞亚群与ＮＣ组比较，ＣＤ８降低（Ｐ＜０．０１），而ＣＤ４／ＣＤ８比值升高（Ｐ＜０．０５）。提示细胞免疫功能紊乱参与ＤＣＭ的病理过程     

C肽、胰岛素在实验性NIDDM大鼠GT实验中的变化

为探讨C肽 (C -P)、胰岛素 (INS)在非胰岛素依赖型糖尿病 (NIDDM )模型糖耐量 (GT)实验中的变化 ,用小剂量尾静脉注射链脲佐菌素 (STZ)加喂高热量饮食形成NIDDM鼠模型 ,对GT实验中C -P、INS的变化进行观察。结果显示 :与对照组比 ,实验组INS升高的高峰时间是在两小时 ,C -P同INS反映一致 ,高峰推迟 (P <0 .0 5 )。提示 :血中C -P测定能准确反映胰腺内生INS水平 ,小剂量注射STZ加喂高热量饮食这种方法形成的NIDDM鼠模型非常理想     

ASS对实验性Ⅱ型糖尿病大鼠胰岛素和C肽分泌作用研究

目的 研究刺五加叶皂甙（ASS）对实验性Ⅱ型糖尿病大鼠胰岛素和C肽分泌作用影响。方法 应用放射免疫学方法对正常组和Ⅱ型糖尿病模型组大鼠（尾静脉注射链尿佐菌素25mg/kg加高脂，高热、高能量喂养）。在给予ASS后其空腹及口服葡萄糖后血浆中胰岛素和C肽变化测定。结果 ASS可增强Ⅱ型糖尿病大鼠胰岛素和C肽分泌，对正常大鼠无影响。结论 ASS可以促进Ⅱ型糖尿病大鼠胰岛素和C肽分泌。     

消渴汤方剂对Ⅱ型糖尿病大鼠胰岛素和C肽分泌的影响

目的　研究消渴汤中药对Ⅱ型糖尿病大鼠胰岛素和C肽水平分泌作用影响。方法　同随机方法将 4 4只Wistar大鼠分为正常和实验组 ,应用放射免疫方法对正常组和Ⅱ型糖悄病模型组大鼠 (尾静脉注射链尿佐菌素 2 5mg/kg加高脂 ,高热 ,高能量喂养 )。在给予消渴汤后其空腹及口服葡萄糖后血浆中胰岛素和C肽水平变化测定。结果　消渴汤可增强Ⅱ型糖尿病大鼠胰岛素和C肽分泌 ,对正常大鼠无影响。结论　消渴汤可以促进Ⅱ型糖尿病大鼠胰岛素和C肽分泌。     

肥胖患者血清瘦素、C-肽和外周脂肪组织中瘦素受体水平的变化分析

目的 :通过对肥胖及伴有 2型糖尿病患者瘦素、C -肽及外周脂肪组织leptin受体表达的研究 ,进一步探讨肥胖及肥胖伴 2型糖尿病患者发生发展的机制。方法 :用放射免疫分析和放射配基结合实验的方法 ,对 91例受检者 (其中肥胖 38例 ,超重 2 3例 ,正常对照 30例 )外周脂肪组织leptin受体的密度及血清中的瘦素、C -肽水平进行检测。结果 :随着BMI的增加 ,瘦素受体密度肥胖组和超重组与正常组比较差异十分显著(p <0 0 1) ,肥胖组与超重组比较有显著性差异 (p <0 0 1) ;而受体与瘦素结合的能力 (Kd值 )没有显著性差异(p >0 0 5 )。三组间的Kd值无差异。从散点分布图可以看出体重指数越大其leptin受体的密度就越小 ,BMI与Bmax相关性 (r=- 0 70 ,p<0 0 1) ;在超重和肥胖伴有 2型糖尿病患者 ,血清中的瘦素和C -肽水平肥胖组比超重组明显升高 ,二者的比值有明显差异 (p <0 0 1) ;血清C -肽增高幅度比瘦素明显 ;血清C -肽水平与体重指数呈正相关。结论 :单纯性肥胖及肥胖伴 2型糖尿病患者血清瘦素、C -肽水平及外周脂肪组织中leptin受体的密度的变化与BMI密切相关 ,肥胖病人所并发的 2型糖尿病与瘦素抵抗和胰岛素抵抗密切相关     

Insulin receptor antibodies in diabetes mellitus

Sera from 80 subjects with IDDM and NIDDM, together with sera from 20 patients with miscellaneous autoimmune conditions and 20 healthy adult subjects were tested for insulin receptor antibodies by (1) inhibition of 125I-insulin binding to EBV-transformed lymphoid cells, and by (2) immunoprecipitation of solubilized insulin receptors in the presence of an excess of mono-specific anti-human IgG or IgM; this test allowed the assessment of the class of antibody activity. Anti-insulin antibodies in the sera were also measured using a double antibody technique. Anti-insulin receptor antibodies were found in 13 of 33 subjects with IDDM and six of 47 with NIDDM. These were principally in the IgM class, and in both groups of diabetics there was a good correlation between % inhibition of insulin binding to intact cells, and % of antibody precipitated by IgM (P less than 0.001), but not by IgG (P greater than 0.1). There was also a good correlation between the % inhibition of insulin binding to intact cells and the daily dose of insulin used in treatment (P less than 0.001). Insulin antibodies were found in seven of 33 subjects with IDDM and six of 12 with NIDDM, all of whom were on insulin treatment. These six subjects were the only ones with NIDDM who also had anti-insulin receptor antibody activity, suggesting that such antibodies may represent auto-anti-idiotype activity. This study shows that autoimmunity in insulin dependent (Type I) diabetes is not limited to islet cells and that such patients also develop antibodies to the insulin receptor. While three out of five patients with relative insulin resistance (requirement greater than 90 u/day) also showed evidence of insulin receptor antibody activity, the clinical significance of these antibodies has yet to be determined.     

Resistance of the aged myocardium to exercise-induced chronic changes in glucose transport related protein content

The effects of acute exercise on myocardial content of glut-1 and glut-4 transporters, insulin and IGF-1 receptors were assessed in control and chronically exercised 24-month-old C57B1/6 mice. Myocardial glut-1, glut-4, insulin receptor (Ins R) and insulin like growth factor-1 receptor (IGF-1 R) protein levels were unaffected by 36 weeks of chronic exercise. However, myocardial protein content of glut-1, but not glut-4, was increased 12 h following an acute exercise bout in control (46%) and chronically exercised (83%) aged animals. This increased glut-1 response following acute exercise occurred despite the finding that the chronic exercise failed to increase cardiac or skeletal muscle oxidative capacity as indicated by no change in citrate synthase activity. Myocardial IGF-1 R content was unaffected by acute exercise whereas Ins R protein content was decreased 12 h following the acute exercise bout in the chronically exercised (-52%) and control (-28%) animals. The effect of acute exercise on the protein content of glut-1 and Ins R was 80 and 84% greater respectively, in the chronically exercised animals. This suggests that the amplitude of the expression of these two proteins may be increased by chronic exercise, thus constituting a form of adaptation.     

测定血清INS、C-P对原发性高血压患者的临床意义

为探讨测定血清胰岛素（INS）,C－肽（C－P）对原发性高血压（EH）患者的应用价值,对32例EH患者的空腹和餐后2小时血糖（BG）、INS、C－P等指标进行测定,计算胰岛素敏感指数（ISI）,并与40名对照组进行比较,结果发现,EH组与对照组空腹血糖无明显差异,而空腹INS及餐后2小时BG、INS、C－P均明显高于对照组（P＜0．01）;胰岛素抵抗、高胰岛素血症比例均明显高于对照组（P＜0．01）。提示EH除血管和血液动力学异常外,尚存在多种物质代谢异常,同时血清INS、C－P的RIA测定在糖尿病以外疾病中的应用前景也很广扩。．     

Antilipolytic effect of insulin in non-insulin-dependent diabetes mellitus after conventional treatment with diet and sulfonylurea

Insulin-induced antilipolysis was investigated in fat cells obtained after an overnight fast and 60 min after glucose ingestion in seven non-obese patients with non-insulin-dependent diabetes mellitus (NIDDM). The study was performed before and after long-term therapy with diet and glibenclamide. After treatment, the antilipolytic potency of insulin in fat cells was threefold enhanced (p less than 0.05) in the fasting state and remained unaltered after glucose ingestion. In untreated NIDDM oral glucose induced a significant (p less than 0.01) increase in insulin sensitivity. In consequence, in the glucose-fed state insulin sensitivity was similar before and after therapy. Adipocyte insulin receptor binding was comparable before and after therapy, both in the fasting state and following glucose intake. In untreated NIDDM, despite relative hypoinsulinemia, plasma glycerol was markedly reduced after oral glucose. After therapy, plasma glycerol was significantly reduced both in the fasting state and following glucose ingestion. At the same time, fasting and glucose-stimulated circulating insulin were significantly (p less than 0.01) increased. It is concluded that conventional antidiabetes therapy in NIDDM mediates a suppression of adipose tissue lipolysis. This seems to be due to an improvement in insulin secretion in combination with a potentiation of the antilipolytic effectiveness of insulin in fat cells in the fasting state, the latter being secondary to post-binding alterations in insulin action.     

非胰岛素依赖型糖尿病胆结石的血脂研究

探讨了非胰岛素依赖型糖尿病的脂肪代谢异常对胆结石发病的影响．设糖尿病胆石组30例、对照组A单纯糖尿病65例及B单纯胆石组30例．测定血脂四项及血浆胰岛素水平，作比较性研究．结果显示：糖尿病胆石组与A组比较，低密度脂蛋白、血浆胰岛素水平(空腹及餐后2小时)升高．相差显著；高密度脂蛋白水平降低．相差显著．与B组比较．血清总胆固醇、甘油三酯，低密度脂蛋白水平升高．相差显著；高密度脂蛋白水平降低．相差显著．提示：脂肪代谢紊乱，特别是脂蛋白代谢异常在非胰岛素依赖型糖尿病人的胆结石形成过程中起重要作用．     

The natural history of impaired glucose tolerance in the Pima Indians

Among 384 Pima Indians with impaired glucose tolerance according to World Health Organization criteria who were followed for 1.6 to 11.5 years (median, 3.3), non-insulin-dependent diabetes mellitus (NIDDM) developed in 118 (31 percent), glucose tolerance remained impaired in 100 (26 percent), and glucose tolerance returned to normal in 166 (43 percent). The cumulative incidence of NIDDM was 25 and 61 percent at 5 and 10 years, respectively. The risk of development of diabetes was 6.3 times (95 percent confidence interval, 3.8 to 10.6) as high as in a normoglycemic control group (n = 752). Variables predicting deterioration to NIDDM were age up to the age of 40, after which increasing age had a beneficial effect; higher plasma glucose levels during fasting and after carbohydrate loading; and higher serum insulin levels after fasting and lower levels after carbohydrate loading, suggesting that insulin resistance and decreased beta-cell responsiveness are important determinants of the clinical outcome of impaired glucose tolerance. Obese subjects had 2.9 times (95 percent confidence interval, 2.0 to 10.9) the incidence of NIDDM as the nonobese. Obesity was not, however, predictive of progression to NIDDM after an adjustment for plasma glucose and serum insulin levels. We conclude that in this population approximately one fourth of subjects with impaired glucose tolerance have NIDDM at five years and two thirds at 10 years (approximately one third revert to normal) and that age and plasma glucose and insulin levels are the best predictors of clinical outcome.