脂蛋白（a）与非胰岛素依赖型糖尿病

为探讨血清脂蛋白（ａ）浓度与非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者慢性并发症的关系，以１００例非糖尿病患者作对照，对１５０例ＮＩＤＤＭ患者的血清脂蛋白（ａ）浓度及其与其他血脂的相关性进行了分析。结果显示，两组的血清脂蛋白（ａ）浓度无明显差异（Ｐ＞０．５），两组的脂蛋白（ａ）与总胆固醇、低密度脂蛋白－胆固醇、甘油三酯、高密度脂蛋白－胆固醇、载脂蛋白Ａ－Ⅰ和Ｂ的浓度无相关性（均Ｐ＞０．１）。糖尿病组并发高血压、大血管和微血管病变者血清脂蛋白（ａ）浓度明显高于无相应并发症者（Ｐ＜０．００１或Ｐ＝０．００２）；血清脂蛋白（ａ）浓度与并发大血管病变和尿蛋白定性阳性者呈正相关（相关系数分别为０．１８５和０．３１６，Ｐ＝０．０２４和Ｐ＜０．００１）。血清脂蛋白（ａ）浓度升高可能是ＮＩＤ－ＤＭ患者冠心病、脑血管病等易患的独立危险因素。     

脂蛋白（a）与非胰岛素依赖型糖尿病代谢控制的关系

为探讨非胰岛素依赖型糖尿病血糖控制对血清脂蛋白浓度的影响，对１０６例ＮＩＤＤＭ和５４例正常对照者的脂蛋白和其它成分进行了分析，结果显示ＮＩＤＤＭ组脂蛋白（ａ）高于对照组。根据糖化血红蛋白水平将ＩＤＤＭ组成三组，三组间脂蛋白无显著性差异。相关分析发现ＮＩＤＤＭ全组脂蛋白与糖化血红蛋白和血糖无相关性。进一步用多元逐步回归分析显示，脂蛋白与糖化血红蛋白无关联。研究结果表明ＮＩＤＤＭ血糖控制对脂蛋白无影响     

脂蛋白(α)与非胰岛素依赖型糖尿病代谢控制的关系

为探讨非胰岛素依赖型糖尿病（ＮＩＤＤＭ）血糖控制对血清脂蛋白（α）浓度的影响，对１０６例ＮＩＤＤＭ和５４例正常对照者的脂蛋白（α）和其它血脂成分进行了分析，结果显示ＮＩＤＤＭ组脂蛋白（α）高于对照组（Ｐ＜０，０１）；根据糖化血红蛋白水平将ＮＬＤＤＭ组分成三组，三组间脂蛋白（α）无显著性差异；相关分析发现ＮＩＤＤＭ全组脂蛋白（α）与糖化血红蛋白和血糖无相关性（Ｐ均＞０．０５）。进一步用多元逐步回归分析显示，脂蛋白（α）与糖化血红蛋白无关联（Ｐ＞０．０５）。研究结果表明ＮＩＤＤＭ血糖控制对脂蛋白（α）无影响。     

年青人的成年发病型糖尿病（MODY）—非胰岛素依赖型糖尿病的…

年青人的成年发病型糖尿病是非胰岛素依赖型糖尿病的一种亚型，但发病年龄偏小，一般认为在２５岁前发病，为常染色体显性遗传性疾病，在流行病学、胰岛素的分泌、敏感性和抵抗性以及临床表现等方面均与非胰岛素依赖型糖尿病及胰岛素依赖型糖尿病都有一定的差异。     

非胰岛素依赖型糖尿病合并冠心病者的胰岛素抵抗

为了解非胰岛素依赖型糖尿病（ＮＩＤＤＭ）病人中胰岛素抵抗与冠心病的关系，对４０例ＮＩＤＤＭ合并冠心病的男病人与３６例未合并冠心病的ＮＩＤＤＭ男病人的血糖、胰岛素、胰岛素敏感性指数（ＩＳＩ）、血脂、载脂蛋白等进行比较，并对其与冠心病的关系进行多因素ｌｏｇｉｓｔｉｃ逐步回归分析，结果显示，ＮＩＤＤＭ病人中的ＩＳＩ与冠心病呈显著负相关（ＯＲ０．２３７，９５％可信区间０．０９０９～０．６１６７，Ｐ＝０．００３２），这种相关独立于年龄、肥胖、血压、血脂等心血管危险因素。提示胰岛素抵抗是非胰岛素依赖型糖尿病病人冠心病发病的独立危险因素。     

非胰岛素依赖型糖尿病与HLA

非胰岛素依赖型糖尿病与ＨＬＡ吴松华，项坤三自７０年代人类白细胞抗原（ＨＬＡ）免疫学分型方法迅速发展，并应用于与人类疾病关系的研究以来，各国学者开展了ＨＬＡ与糖尿病，尤其与Ⅰ型糖尿病（ＩＤＤＭ）发病关系的研究。曾发现西方白种人中１１号染色体胰岛素基因５...     

非胰岛素依赖型糖尿病肾病变探讨

非胰岛素依赖型糖尿病肾病变探讨叶蓉绍，汤金娣糖尿病肾病变（ＤＮ）是糖尿病的主要并发症之一，临床诊断主要依据持续蛋白尿的出现，准确诊断要依靠活组织检查［１］。我们选择糖尿病病情稳定而临床有持续蛋白尿的非胰岛素依赖型糖尿病（ＮＩＤＤＭ）病人作肾活组织检查...     

非胰岛素依赖型糖尿病和糖耐量低减患者的胰岛素敏感性及其相关因素研究

为评价糖耐量异常者的胰岛素敏感性改变及其有关因素，对５７２例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）、６４７例糖耐量低减（ＩＧＴ）和５４３名正常对照者进行了研究。结果显示，空腹血浆胰岛素（ＦＩｎｓ）水平和高胰岛素血症的百分率，在ＮＩＤＤＭ组＞ＩＧＴ组＞正常对照组（Ｐ＜０．０１）。胰岛素敏感性指数（ＩＳＩ）［－ｌｎ（ＦＩｎｓ×空腹血糖）］从大到小的排列顺序为：正常对照组、ＩＧＴ组，新诊断糖尿病组和原诊断糖尿病组（Ｐ＜０．０１）。各组肥胖者的ＩＳＩ小于非肥胖者（Ｐ＜０．０１）。单因素相关性分析显示，各组ＩＳＩ与体重指数（ＢＭＩ）呈负相关，与高密度脂蛋白胆固醇呈正相关。糖尿病组和ＩＧＴ组的ＩＳＩ与血压也呈负相关。多元逐步回归分析显示，ＩＳＩ与ＢＭＩ呈负相关，部分与血压、血脂也有相关性。提示糖耐量异常者伴有高胰岛素血症和胰岛素抵抗，ＩＳＩ与血管病变的危险因素有相关性。     

200例老年人非胰岛素依赖型糖尿病肾病的临床分析

２００例老年人非胰岛素依赖型糖尿病肾病的临床分析姬平，牟善初，余霞君，李丽一、临床资料１９７８～１９９２年住院及随访的老年人非胰岛素依赖型糖尿病（ＮＩＤＤＭ）肾病２００例，男１９３例，女７例；年龄６０～９０岁，平均７３．６岁；继发糖尿病肾病共４６例，...     

非胰岛素依赖型糖尿病遗传学上性别差异的临床研究

通过645例患者的家族史调查进行了对非胰岛素依赖型糖尿病在遗传学上是否存在性别差异的临床研究,报道如下。 一、对象与方法 对1993年7月至1994年3月我院门诊及住院糖尿病病人逐一进行家族史调查、登记;并对1992年、1993年住院的糖尿病病人进行回顾性资料分析。其中一级亲属糖尿病史均已明确诊断者方在统计之列。住院病人部分资料可疑者进行了家访调查。 全部有关资料均经统计学X~2检验或t检验。考虑到本研究对象女性患者稍多,对检验结果进行了校正。     

2型糖尿病患者血清脂蛋白(a)水平及其与冠心病的关系

目的　探讨 2型糖尿病患者血清脂蛋白 (a) [Lp(a) ]水平及其与冠心病的关系。方法　选择 90例 2型糖尿病及 6 8例健康对照者测定其血清Lp(a)、总胆固醇 (TC)、甘油三酯 (TG)、高密度脂蛋白胆固醇 (HDL C)水平 ;计算低密度脂蛋白胆固醇 (LDL C)水平及TC、TG、LDL C与HDL C比值。结果　 (1)糖尿病组血清Lp(a)水平与对照组比较差异无显著性意义 (P >0 .0 5 )。 (2 )将 2型糖尿病患者分为糖尿病伴冠心病和单纯糖尿病亚组后发现 :①糖尿病伴冠心病亚组血清Lp(a)水平明显高于单纯糖尿病亚组 [(2 3.78± 2 3.73)mg/dlvs (13.31± 10 .6 6 )mg/dl;P <0 .0 1]及对照组 [(2 3.78± 2 3.73)mg/dlvs (16 .2 8± 17.95 )mg/dl;P <0 .0 5 ];②糖尿病伴冠心病亚组血清Lp(a)水平与LDL C呈正相关关系 (r =0 .32 16 ,P <0 .0 5 )。结论　 2型糖尿病患者血清Lp(a)水平增高可能与冠心病发病有密切关系。     

Plasma lipoprotein(a) concentration and phenotypes in diabetes mellitus

Summary Patients with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus are at increased risk of developing atherosclerotic vascular diseases. A variety of lipoprotein abnormalities have been described as being associated with this increased risk. In this study, apo(a) isoform frequencies and lipoprotein(a) [Lp(a)] concentrations were determined in Type 1 and Type 2 diabetic patients in order to investigate a possible contribution of Lp(a) to the increased risk for atherosclerosis in diabetes. No significant differences in plasma Lp(a) concentrations were found in two ethnically different populations (Austrians from the province of Tyrol and Hungarians from Budapest) in either type of diabetes when compared to respective control groups (91 Type 1 and 112 Type 2 diabetic patients vs 202 control subjects in the Hungarian study and 44 Type 1 diabetic and 44 Type 2 diabetic vs 125 control subjects in the Austrian study). There were also no significant apo(a) isoform frequency differences between both patient groups and control subjects in the two study groups. These data, obtained from two large ethnically different populations, provide no evidence of a contribution of Lp(a) to the increased risk for atherosclerosis in diabetes.     

Lipids and lipoprotein(a) concentrations in Pakistani patients with type 2 diabetes mellitus

AIM: The aim of the present study was to analyze serum lipoprotein(a) [Lp(a)] levels in Pakistani patients with type 2 diabetes mellitus (DM) and to find correlations between clinical characteristics and dyslipidaemias in these patients. METHODS: Fasting blood samples were analyzed for Lp(a), total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), glucose and glycosylated haemoglobin (HbA1c) in 68 Pakistani patients with type 2 DM and 40 non-diabetic healthy control subjects. RESULTS: Lp(a) levels were significantly raised in diabetics as compared to the control group. No correlation of Lp(a) was seen with age, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP) and fasting glucose. There was a positive correlation of BMI to SBP and DBP. There was a significant positive correlation between Lp(a) and total cholesterol and LDL-c. No correlation of Lp(a) was observed with HDL-c, triglycerides and glycosylated haemoglobin (HbA1c). CONCLUSION: The present study led us to conclude that serum Lp(a) levels are significantly raised in type 2 DM and have a positive correlation with serum total and LDL-c levels.     

The effect of long-term glycaemic control on serum lipoprotein(a) levels in patients with Type 2 diabetes mellitus.

AIMS: To examine whether long-term glycaemic control affects lipoprotein(a) (Lp(a)) levels in patients with Type 2 diabetes mellitus. METHODS: Eighty-nine Type 2 diabetic patients (38 men, 51 women) were recruited from the diabetes clinic. Based on HbA1c concentrations at baseline, patients were divided into two groups: those with HbA1c < 8.0% (n =45) and those with HbA1c > or = 8.0% (n=44). Comparisons of Lp(a) levels were made between both groups. The effect of long-term glycaemic control on Lp(a) levels was investigated in a subgroup of 20 patients, selected from those with baseline HbA1c > or = 8%. All these patients were treated with a goal of HbA1c <7%. RESULTS: Lp(a) levels were not significantly different between those with HbA1c< 8.0% and those with HbA1c, > or = 8.0%. No correlation between Lp(a) and HbA1c or fasting blood glucose levels was noted in diabetic patients as a whole. After 2 years of intensive glycaemic control, all patients exhibited remarkable improvement of therapy: their average HbA1c levels were 6.5 +/- 0.7%, being < 7% in 70% of patients. However, no change in Lp(a) levels were observed after 2 years (19.5 +/- 14.8-21.4 +/- 13.4 mg/dl, P = 0.390). CONCLUSION: These results indicate that improvement of glycaemic control does not affect serum Lp(a) levels in patients with Type 2 diabetes mellitus.     

The relationship between lipoprotein(a) and the complications of diabetes mellitus

The risk of cardiovascular disease is increased approximately two- to four-fold in patients with diabetes mellitus compared with non-diabetic controls. The nature of this increased risk cannot be completely explained by the contribution of traditional risk factors. As such, there has been a great deal of interest in assessing the role of lipoprotein(a) (Lp(a)), an LDL-like lipoprotein, in the vascular complications of diabetes. Although numerous studies in the non-diabetic population have demonstrated an association between elevated plasma Lp(a) concentration and risk for atherosclerotic disorders, the contribution of Lp(a) to the enhanced risk of vascular disease in the diabetic population is not clearly defined. Herein we review the structure and potential functions of Lp(a), the determination of Lp(a) levels, and the epidemiological evidence supporting its role in coronary heart disease and address the following controversial questions regarding the role of Lp(a) in diabetes mellitus: (1) are plasma Lp(a) levels and phenotype distributions altered in type 1 (insulin-dependent) diabetes mellitus and type 2 (non-insulin-dependent) diabetes mellitus and does the degree of metabolic control influence Lp(a) levels in these patients; (2) what is the relationship between Lp(a) and renal disease in patients with diabetes mellitus; (3) do increased plasma Lp(a) concentrations in patients with diabetes contribute to the vascular complications of this disease; and (4) can the atherogenicity of Lp(a) in diabetes be enhanced in the absence of elevated levels of this lipoprotein due to biochemical modifications. Received: 11 January 2002 / Accepted in revised form: 9 December 2002 Correspondence to S.M. Marcovina     

冠心病合并非胰岛素依赖型糖尿病患者冠状动脉造影特点

目的 探讨冠心病（ＣＨＤ）合并非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者的临床及冠状动脉（冠脉）造影特点。方法 对冠脉造影病例进行临床表现和血管造影资料对照分析。结果 冠心病合并ＮＩＤＤＭ者倾向于聚集多种心血管危险因素（高血压、血脂异常）。ＮＩＤＤＭ对女性的血脂异常影响似乎更为显著。与非糖尿病的冠心病虱相比,冠心病合并ＮＩＤＤＭ者不稳定心绞痛多见,且女性心肌梗死危险性增高。其冠脉血管受累程度高且弥漫性     

Serum lipoprotein(a) concentrations and apolipoprotein(a) phenotypes in the families of NIDDM patients

Summary We studied the quantitative and qualitative characteristics of lipoprotein(a) [Lp(a)] as a function of apolipoprotein(a) [apo(a)] phenotype in 87 members (42 males, 45 females) of 20 diabetic families, 26 of whom were diagnosed with non-insulin-dependent diabetes mellitus (NIDDM) with moderate glycaemic control (HbA_1c7.1±1.2%). Apo(a) phenotyping was performed by a sensitive, high-resolution technique using SDS-agarose/gradient PAGE (3–6%). To date, 26 different apo(a) phenotypes, including a null type, have been identified. Serum Lp(a) levels of NIDDM patients and non-diabetic members of the same family who had the same apo(a) phenotypes were compared, while case control subjects were chosen from high-Lp(a) non-diabetic and low-Lp(a) non-diabetic groups with the same apo(a) phenotypes in the same family. Serum Lp(a) levels were significantly higher in NIDDM patients than in non-diabetic subjects (39.8±33.3 vs 22.3±19.5 mg/dl, p<0.05). The difference in the mean Lp(a) level between the diabetic and non-diabetic groups was significantly (p<0.05) greater than that between the high-Lp(a) non-diabetic and low-Lp(a) non-diabetic groups. An analysis of covariance and a least square means comparison indicated that the regression line between serum Lp(a) levels [log Lp(a)] and apo(a) phenotypes in the diabetic patient group was significantly (p<0.01) elevated for each apo(a) phenotype, compared to the regression line of the control group. These data, together with our previous findings that serum Lp(a) levels are genetically controlled by apo(a) phenotypes, suggest that Lp(a) levels in diabetic patients are not regulated by smaller apo(a) isoforms, and that serum Lp(a) levels are greater in diabetic patients than in non-diabetic family members, even when they share the same apo(a) phenotypes.Abbreviations Lp(a) Lipoprotein(a) - apo(a) apolipoprotein(a) - NIDDM non-insulin-dependent diabetes mellitus - TC total cholesterol - LDL low density lipoprotein - TG triglycerides - HDL-C high density lipoprotein-cholesterol - LDL-C low density lipoprotein-cholesterol - PBS phosphate buffered saline The first two authors contributed equally to this work     

The role of lipoprotein(a) in the vascular complications of diabetes mellitus

Abstract. Lipoprotein(a) has been identified as an independent risk factor for atherosclerotic vascular disease in non-diabetic populations. Because of its potential role in the pathogenesis of both microvascular and macrovascular complications in diabetes, there have recently been many reports on lipoprotein(a) in diabetic populations. Some studies indicate an association between elevated lipoprotein(a) and macro-vascular disease in non-insulin-dependent diabetes mellitus (NIDDM), but this link has not been found with insulin-dependent diabetes mellitus (IDDM). In IDDM, elevated lipoprotein(a) has been found in groups with diabetic nephropathy and retinopathy, raising the possibility that it plays a causative role. The relationship between glycaemic control and the lipoprotein(a) level has not been fully resolved. Most studies have not found any connection in NIDDM, but some found higher lipoprotein(a) levels in hyper-glycaemic IDDM patients. Potentially, lipoprotein(a) is an important factor linking the microvascular and macrovascular complications of diabetes.     

Apolipoprotein (a) levels in type 1 and type 2 diabetes mellitus

Type 1 and type 2 diabetes mellitus are both characterized by increased cardiovascular mortality and morbidity. Since several reports have indicated that apolipoprotein (a) [apo (a)] levels are positively associated with an increased risk of macrovascular disease, we investigated whether apo (a) levels are elevated in both types of diabetes mellitus and may thus represent an independent risk factor for atherosclerotic disease. Apo(a) concentrations in type 1 diabetic patients were not significantly different from matched controls (276±78 vs 149±46 units/l). Type 2 diabetic patients had considerably higher levels of apo (a) than matched controls (471±89 vs 221±61 units/l,P=0.06), though the difference was not statistically significant. However, concentrations of apo (a) were above 300 units/l in 36% of type 1 and 67% of type 2 diabetic patients, but in only 14% and 25% respectively of matched control subjects. Plasma triglycerides were positively and independently correlated with apo (a) levels in both diabetic and non-diabetic subjects. On the other hand, no significant correlation was found between apo (a) levels and glycosylated haemoglobin, total cholesterol or high density lipoprotein cholesterol in any of the groups studied. In conclusion, apo (a) levels are not significantly elevated either in type 1 or type 2 diabetic patients without proteinuria and in moderate metabolic control; however, levels above 300 units/l were 2.6 times more frequent in both types of diabetes mellitus than in carefully age-, sex-, and weight-matched control subjects.