高血糖与醛糖还原酶的激活

应用荧光法、Ｃ１８反相高压液相层析和气相色谱法分别测定１７例正常人和３２例Ⅱ型糖尿病患者（１７例有并发症）红细胞内的醛糖还原酶活性、某些核普酸和糖醇浓度。结果显示：Ⅱ型糖尿病患者红细胞内醛糖还原酶的活性高于正常人；有并发症患者的酶活性又高于无并发症患者，证明高血糖能激活醛糖还原酶，激活程度与血糖浓度呈正相关。患者红细胞内ＮＡＤＰ＋、山梨醇和果糖的浓度高于正常对照；ＮＡＤＰＨ和ＮＡＤ＋浓度低于正常对照，而此５项指标在两组患者间差异无显著性。     

非胰岛素依赖型糖尿病患者红细胞膜ATP酶活力和细胞内离子水平变化

测定20例正常人及40例 NIDDM 患者红细胞膜 ATP 酶活力和红细胞内离子浓度。结果NIDDM 患者 Na~+-K~+-ATP 酶、Ca~(2+)-ATP 酶活力明显低于正常人(P 均<0.001),Mg~(2+)-ATT 酶活力无明显改变(P>0.05);NIDDM 患者红细胞内[Na~+]、[Ca~(2+)]明显高于正常人(P 分别<0.001和0.01),[Mg~(2+)]明显低于正常人(P<0.001),[K~+]无明显变化(P>0.05)。上述变化在无血管病者就已出现,有血管病者更加明显。     

非胰岛素依赖型糖尿病病人红细胞镁浓度变化及镁对红细胞变形能力的影响

检测了６４例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）病人红细胞镁（Ｅ－Ｍｇ（２＋））浓度变化，同时观察了镁在体外对ＮＩＤＤＭ病人红细胞变形能力（ＥＤ）、红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶活性、Ｅ－Ｍｇ（２＋）和红细胞钙（Ｅ－Ｃａ（２＋））浓度的影响。结果显示，ＮＩＤＤＭ病ＨＥ－Ｍｇ（２＋）浓度较对照组明显降低（Ｐ＜０．００１），有血管病变者降低更明显。ＮＩＤＤＭ病人红细胞与镁共同孵育后，红细胞滤过指数（ＩＦ）、Ｅ－Ｃａ（２＋）明显降低，Ｅ－Ｍｇ（２＋）和红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶活性明显增高，与孵育前比较差异有极显著性（Ｐ＜０．００１），与对照组比较差异无显著性（Ｐ＞０．０５）。提示镁对改善ＮＩＤＤＭ病人血液流变学、减少血管病变的发生有重要意义。     

Ghrelin对PI3K/Akt抑制剂预处理大鼠中枢血压调节及NADPH表达的影响

目的 研究食欲刺激素(ghrelin)对PI3K/Akt抑制剂预处理大鼠中枢血压调节及血管烟酰胺腺嘌呤二核苷酸磷酸(NADPH)表达的影响.方法 选取10~12周龄雄性SD大鼠18只,腹腔内注射麻醉,股动、静脉插管,侧脑室内插管.随机分为3组,人工脑脊液(aCSF)对照组,ghrelin组,PI3K抑制剂(wortmannin)预处理组,每组6只.aCSF组侧脑室内注射aCSF(10 μL);ghrelin组侧脑室内注射aCSF(10 μL),10 min后侧脑室内注射食欲刺激素(50 pmol/10 μL);wortmannin预处理组侧脑室内注射wortmannin (20 nmol/10 μL),10 min后侧脑室内注射食欲刺激素(50 pmol/10 μL).观察各组血压、心率的变化.用酶联免疫吸附法,实验结束后测定NADPH浓度.结果 Ghrelin组平均动脉压(MAP)最大下降幅度(-12.3±2.6)mmHg,心率(HR)最大下降幅度(-29.5±13.4) bpm,与aCSF组相比,差异具有统计学意义(P<0.01, P<0.05).wortmannin预处理组侧脑室内注射食欲刺激素后MAP最大下降幅度(-4.0±2.7)mmHg,与ghrelin组相比,差异具有统计学意义(P<0.01);与aCSF组比较,差异无统计学意义.在延髓和下丘脑中,ghrelin组NADPH浓度为(67.3±8.2)μmol/L和(67.5±7.2) μmol/L,均明显高于aCSF组(P<0.01);wortmannin预处理组与aCSF对照组及ghrelin组比较,差异均无统计学意义.结论 ghrelin通过PI3K/Akt信号传导通路引起降压作用并上调NADPH表达.     

Silybin decreases erythrocytic sorbitol level and improves peripheral nerve conduction velocity in patients with non-insulin dependent diabetes mellitus

The effects of silybin on erythrocytic sorbitol level and peripheral nerve conduction velocity were studied in 14 cases of non-insulin dependent diabetes mellitus (NIDDM). After oral administration of silybin 231 mg/day for 4 weeks, no blood glucose change was observed in patients with NIDDM, while the erythrocytic sorbitol level was significantly decreased from 72.55±21.61 to 39.53±14.94 nmol/g · Hb (P<0.01). At the same time, peripheral nerve conduction velocity was also improved. These results indicate that silybin is an effective aldose reductase inhibitor which can improve the disorder of polyol pathway in NIDDM patients and prevent chronic complications of diabetes.     

川芎嗪对早期糖尿病大鼠股骨头组织中醛糖还原酶、一氧化氮、一氧化氮酶及钠-钾-ATP酶的影响

目的探讨川芎嗪对早期糖尿病(DM)大鼠股骨头中醛糖还原酶(AR)、一氧化氮(NO)、一氧化氮酶(NOS)系统及钠-钾-ATP酶(Na+-K+-ATPase)的影响。方法选择SD大鼠,随机分为对照组、DM模型组和川芎嗪组。一次性腹腔注射链脲佐菌素(STZ)60 mg.kg-1诱发糖尿病,分别于30 d和60 d测定各组大鼠股骨头匀浆中的NO含量、NOS活性、Na+-K+-ATPase及AR含量。结果30 d、60 d时DM组的NO、NOS和Na+-K+-ATPase均低于对照组和川芎嗪组(P<0.01),AR均高于对照组和川芎嗪组(P<0.01);30 d时川芎嗪组NO、NOS、AR和Na+-K+-ATPase与对照组比较无明显差异(P>0.05);60 d时川芎嗪组NO、NOS和Na+-K+-ATPase均低于对照组(P<0.01),AR高于川芎嗪组(P<0.01);60 d时DM组和川芎嗪组大鼠股骨头匀浆中NO含量和NOS活性和Na+-K+-ATPase均明显低于30 d时(P<0.01),AR均高于30 d时(P<0.01)。结论川芎嗪能逆转股骨头组织中AR、NO、NOS及Na+-K+-AT-Pase活性,对防治早期DM大鼠股骨头病变有一定的效果。     

冠心病患者并发Ⅱ型糖尿病所占比例的胰岛素水平分析

目的探讨冠心病(CHD)患者中,发生Ⅱ型糖尿病(NIDDM)的比例及其临床意义.方法用放射免疫分析法检测166例临床已确诊为冠心病患者和24例健康者的空腹及餐后2 h血胰岛素水平,根据病史、症状、血糖及胰岛素的水平,将166例冠心病患者划分为冠心病合并Ⅱ型糖尿病(CHD合并NIDDM)组和冠心炳未合并Ⅱ型糖尿病组(CHD未合并NIDDM).结果100例CHD合并NIDDM组空腹及餐后2 h的血胰岛素水平都极显著高于对照组(P＜0.01).Ⅱ型糖尿病患者所占的比例达60.4%.66例CHD未合并NIDDM组空腹及餐后胰岛素水平亦明显高于对照组(P＜0.01).结论在冠心病患者中存在高血胰岛素血症,但以合并Ⅱ型糖尿病所占比例为明显较高.检测血胰岛素,对冠心病患者合并糖尿病的预防、诊断、疗效评估均有重要的临床意义.     

Changes in RBC Ca2(+)-ATPase activity and red-cell calcium concentration during dialysis in patients with uremia

The changes of RBC Ca2(+)-ATPase activity and red cell calcium concentration during dialysis were observed in 19 patients with uremia. The results showed that in 12 patients treated by haemodialysis the RBC Ca2(+)-ATPase activity was lowered an average of 35 U than that in the controls (P less than 0.001); whereas red cell calcium was increased about 5 times (P less than 0.001). After a four-hour haemodialysis, the Ca2(+)-ATPase activity increased 20 U (P less than 0.05); and red cell calcium decreased 45 mumol/L cells (P less than 0.05). In 7 patients treated by CAPD the RBC Ca2(+)-ATPase activity was reduced to 60% of that in the controls (P less than 0.001); and red cell calcium was about 5 times as high as that in the controls (P less than 0.001). After one month of CAPD, the Ca2(+)-ATPase activity increased only 10 U (P greater than 0.05); but red cell calcium decreased 66 mumol/L cells (P less than 0.01).     

糖尿病患者血清层粘连蛋白水平及其影响因素的探讨

目的：为探讨血清层粘连蛋白（Ｌａｍｉｎｉｎ,ＬＮ）与糖尿病微血管病变的关系,研究糖尿病患者血清ＬＮ的影响因素。方法：用放免法测定７６例２型糖尿病患者和３８例正常对照者的血清ＬＮ浓度。结果：糖尿病患者血清ＬＮ显著高于正常对照（分别为１６８．７６±２７．８４ｎｇ／ｍｌ和１４９．０９±２８．８４ｎｇ／ｍｌ,Ｐ＜０．０１有微血管病变患者显著高于无微血管病变患者（分别为 １７４．９７±２７．１４ｎｇ／ｍｌ和１５８．１２±２６．１２ｎｇ／ｍｌ　Ｐ＜０．０２）,糖尿病视网膜病变（ＤＲ,ｎ＝４１,１７５．６２±２６．５６ｎｇ／ｍｌ）和糖尿病肾病（ＤＮ, ｎ＝２８, １７９．５９±２９．６６ｎｇ／ｍｌ）患者血清 ＬＮ分别显著高于无 ＤＲ（ｎ＝３５,１６０．７１±２７．１２ｎｇ／ｍｌ）和无ＤＮ（ｎ＝４８,１６０．５３±２４．１１ｎｇ／ｍｌ）的患者（Ｐ＜０．０５,Ｐ＜０．０１）。同时伴有ＤＲ和ＤＮ患者血清ＬＮ高于单有ＤＲ或单有ＤＮ患者。多元逐步回归分析提示糖尿病患者血清ＬＮ浓度增高的程度与其糖尿病病程长短关系密切。糖尿病患者血清ＬＮ与血清ＩＶ型胶原、血清结合珠蛋白水平呈正相关（Ｒ＝０ ５３,Ｐ＜０．００１和Ｒ＝０．４０,Ｐ＜０．０１）     

ORIGINAL ARTlCLES Silybin Decreases Erythrocytic Sorbitol Leveland Improves Peripheral Nerve Conduction Velocity in Patients with No

ＯＲＩＧＩＮＡＬＡＲＴｌＣＬＥＳＳｉｌｙｂｉｎＤｅｃｒｅａｓｅｓＥｒｙｔｈｒｏｃｙｔｉｃＳｏｒｂｉｔｏｌＬｅｖｅｌａｎｄＩｍｐｒｏｖｅｓＰｅｒｉｐｈｅｒａｌＮｅｒｖｅＣｏｎｄｕｃｔｉｏｎＶｅｌｏｃｉｔｙｉｎＰａｔｉｅｎｔｓｗｉｔｈＮｏｎ－ｌｎｓｕｌｉ...     

胰岛素受体底物—1和葡萄糖转运蛋白基因多态性与糖尿病及糖尿 …

目的 探讨胰岛素受体底物－１（ＩＲＳ－１）和葡萄糖转运蛋白（ＧＬＵＴ１）的基因多态性与糖尿病及其糖尿病肾病的关系。方法 应用ＰＣＲ－＝ＲＦＬＰ方法对１３１例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者ＩＲＳ－１和ＧＬＵＴ１基因多态性进行了观察,并结合肾脏病变、体重指数（ＢＭＩ）和胰岛素敏感指数（ＩＳＩ）进行了分析。结果ＩＲＳ＿１基因多态性在ＮＩＤＤＭ和正常人中的分布没有明显差异。ＮＩＤＤＭ患者ＧＬＵＩ１     

醛糖还原酶的研究进展

醛糖还原酶是醛-酮还原酶超家族的一员,广泛存在于血管、肾脏、心脏、脑、骨骼肌、视网膜、胎盘、神经等组织中。它以烟酰胺腺嘌吟二核苷磷酸（NADPH）为辅酶催化多种醛、酮类物质还原为醇。除促进糖尿病并发症发生外,还参与多种氧化应激性疾病,参与细胞信号转导和细胞增殖过程。     

氨基胍对腹膜间皮细胞醛糖还原酶活性的影响

目的观察氨基胍对腹膜间皮细胞醛糖还原酶活性的影响，探讨氨基胍对腹膜间皮细胞醛糖还原酶的调节作用。方法采用人的网膜作为细胞来源，胰蛋白酶-EDTA消化法进行人腹膜间皮细胞的分离、培养，间接免疫荧光法对第二代细胞进行鉴定；用生长期细胞进行实验，培养6d后测AR活性；应用紫外分光光度计记录NADPH在340nm处的吸光值测定醛糖还原酶活性。结果实验组氨基胍组醛糖还原酶的活性与对照组比较仅略下降，无显著性差异。结论氨基胍并不能明显地抑制腹膜间皮细胞醛糖还原酶的活性。     

家族性Ⅱ型糖尿病家系中非糖尿病一级亲属的高胰岛素血症与胰 …

目的 探讨家族性非胰岛素依赖型糖尿病（ＮＩＤＤＭ）家系中非糖尿病（ＤＭ）一级亲属的血浆胰岛素水平及胰岛素敏感性。方法 对家族性ＮＩＤＤＭ家系啡 ＤＭ一级亲属９７人和健康对照５５人作标准口服葡萄耐量试验（ＯＧＴＴ）,测定各时点的血糖和血浆胰岛素,并由此计算ＯＧＴＴ葡萄糖、胰岛素曲线下面积比（ＳＧＩ）和胰岛素敏感性指数（ＩＳＩ）来反映机体的胰岛素敏感性。结果 在年龄、体重指数（ＢＭＩ）及性别构成比可比     

2型糖尿病微血管病变患者脂蛋白(α)的变化

目的：探讨２型糖尿病人血清脂蛋白（α）水平与发生微血管病变的关系。方法：测定９１例糖尿病人,包括４４例伴微血管病变和４７例未发生微血管病变者的血清脂蛋白（α）（Ｌｐ（α）,ＡｐｏＡ,ＡｐｏＢ,ＴＣ,ＴＧ;血ＨｂＡｌ;尿ＮＡＧ和ＮＡＧ Ｂ等指标,与３２例对照组进行比较。结果：微血管病变的糖尿病人血清Ｌｐ（α）显著高于对照组。糖尿病肾脏并发症患者Ｌｐ（α）水平与ＴＣ（ｒ＝０．２３,Ｐ＜００５）,ＡＥＲ（ｒ＝０．６２,Ｐ＜０．０１）,ＮＡＧ Ｂ（ｒ＝０．５１,Ｐ＜００１）和ＮＡＧＩ（ｒ＝０．４１,Ｐ＜００５）呈现相关。结论：测定Ｌｐ（α）对辅助诊断糖尿病微血管病变有较好的临床价值。     

G6PD--an old bottle with new wine

The major role of glucose-6-phosphate dehydrogenase (G6PD) is to generate reduced nicotinamide adenine dinucleotide phosphate (NADPH), which is indispensable to reductive metabolism and maintenance of cellular redox homeostasis. Most advances in this field have been made in the pathophysiology of G6PD-deficient erythrocytes and the molecular characterization of different G6PD variants. Recently, numerous studies have shown the importance of G6PD in cell growth, development and disease progression.     

Effect of ke-tang-Ling administration on the function of pancreatic islets cells in non-insulin-dependent diabetes mellitus

Radioimmunoassay methods were modified for insulin(IRI), C-peptide (IRCP) and glucagon (IRG) in the clinical investigation on normal subjects and 38 patients with non-insulin-dependent diabetes mellitus (NIDDM). In the control group, the peaks of glucose and IRI appeared 1 hour after glucose was taken. IRCP peak, however, appeared 1 hour later. IRG showed its maximum value on fasting and then reached its lowest point at the second hour after glucose loading. The authors' interests were focused on the changes of blood glucose, IRI, IRCP, and IRG in oral glucose tolerance test (OGTT) before and after Ke-Tang-Ling (KTL) was administered in NIDDM. The results demonstrate that the glucose levels and undercure areas at various phases in OGTT were significantly decreased (P less than 0.01) in comparison of before and after the treatment with KTL in NIDDM (including obese and non-obese groups). In non-obese group, however, IRI, IRCP, and their undercure were remarkably increased (P less than 0.01). In obese group their values were decreased. It suggests that KTL plays a therapeutic role in decreasing blood glucose in non-obese NIDDM. The mechanism involved in this process may be related to its stimulating effect. IRG levels were decreased also (P less than 0.01) after the treatment with KTL in both obese and non-obese NIDDM, suggesting an inhibitory effect on glucagon secretion from alpha cells in pancrease.     

The mutation of insulin receptor substrate-1 gene in Chines e patients with non-insulin-dependent diabetes mellitus

Objective To identify the relationship between mutation in the insulin receptor substrate-1 (IRS-1) gene and the incidence of non-insulin-dependent diabetes mellitus (NIDDM) in the Chinese population. Methods Samples were obtained from 68 Chinese patients with NIDDM and 68 control subjects. The +1700～+4437 bp fragment of the IRS-1 gene was screened by polymerase chain reaction (PCR)-single strand conformation polymorphism (SSCP) analysis. All SSCP variations were submitted to DNA sequence analysis. Results Two amino acid variations ［GGG →AGG(G(971) R) and CCT→TCT(P(1079) S)］ and 3 silent mutations ［GAT→GAC(D(422) D), CCA→CCC(P(737) P) and GCA→GCG(A(804) A)］ were identified, among which the CCA→CCC(P(737) P) and CCT→TCT(P(1079) S) have not been previously reported. All five variations were found in Chinese patients with NIDDM, while GCA→GCG(A(804) A) was the only one found in control subjects. The overall incidence of the five variations in Chinese patients with NIDDM were much higher than that in control subjects (38.2% vs 7.4%, χ(2)=18.42,P&lt;0.01). The most common polymorphism in the Chinese population was GCA→GCG(A(804) A), and its frequency was significantly higher in Chinese patients with NIDDM than in controls (26.5% vs 7.4%, χ(2)=8.84,P&lt;0.01). The homozygotes of the variation in patients with NIDDM and control subjects were 8.8% and 1.5%, respectively (χ(2)=2.41,P&gt;0.05). Conclusion These results indicate that there may be a relation between these nucleotide variations of IRS-1 gene and Chinese patients with NIDDM     

糖尿病患者红细胞膜Na~＋－K~＋－ATPase、Ca~（2＋）－ATPase活性变化

目的探讨糖尿病患者红细胞膜ＡＴＰａｓｅ活性的变化。方法１７例胰岛素依赖型（ＩＤＤＭ）和４８例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者红细胞膜Ｎａ~＋－Ｋ~＋－ＡＴＰａｓｅ、Ｃａ~（２＋）－ＡＴＰａｓｅ活性分别用改良的Ｈａｎａｈａｎ法和Ｌｕｔｈｒａ法测定，并设相应年龄对照组。统计方法用ｔ检验和直线相关分析。结果ＮＩＤＤＭ患者红细胞膜Ｎａ~＋－Ｋ~＋－ＡＴＰａｓｅ、Ｃａ~（２＋）－ＡＴＰａｓｅ活性分别下降了２４．３３％和１７．１１％，ＮＩＤＤＭ患者则分别下降２１．２４％和１６．４２％。两组糖尿病患者ＡＴＰａｓｅ活性均与糖化血红蛋白呈负相关，与年龄、空腹血糖或胰岛素水平无相关。结论糖尿病患者均有红细胞膜Ｎａ~＋－Ｋ~＋－ＡＴＰａｓｅ、Ｃａ~（２＋）－ＡＴＰａｓｅ活性下降，其原因与慢性高血糖有关。     

L-精氨酸对糖尿病大鼠坐骨神经损伤的保护作用

目的：探讨L-精氨酸（L-Arg）对糖尿病（DM）大鼠坐骨神经损伤的保护作用及其机制。方法：用链脲佐菌素制备糖尿病模型。SD大鼠随机分为正常对照组（NC组）、DM组、L-Arg治疗组（L-Arg组）。L-Arg治疗12周后，测定三组大鼠血清、坐骨神经组织一氧化氮（N0）含量和一氧化氮合酶（NOS）活性及血浆内皮素-1（ET-1）、降钙素基因相关肽（CGRP）含量，以及坐骨神经组织Ca^2＋-ATPase、Na^＋-K^＋-ATPase活性及神经元型NOS（nNOS）、醛糖还原酶（AR）基因的表达。结果：DM组大鼠血清、坐骨神经NO含量和NOS活性、血浆CGRP含量及坐骨神经Ca^2＋-ATPase、Na^＋-K^＋-ATPase活性和nNOS mRNA的表达均明显低于NC组（P〈0．01或P〈0．05），而血浆ET-1含量、坐骨神经AR mRNA的表达均明显高于NC组（均P〈0．01）；经L—Arg治疗后，上述改变逆转，与DM组比较差异有显著性（P〈0．01或P〈0．05）。结论：L—Arg对DM大鼠坐骨神经损伤具有一定的保护作用，其机制可能与改善神经血供及抑制多元醇代谢途径有关。