2型糖尿病血管并发症影像评价的研究进展

2型糖尿病的患病率逐年上升,且逐渐年轻化,是危及人类健康、造成经济负担的主要疾病。全身性大小血管病变是2型糖尿病的主要并发症之一,也是糖尿病心血管疾病发病和死亡的主要原因。相关研究表明,早期影像评价可在糖尿病血管并发症症状或靶器官功能障碍出现之前检测到显著的变化,为疾病的早期干预、疗效评估及预后分析提供影像学证据。现就各影像技术在血管病变的成像特点、作用及未来发展进行综述,深入认识各影像学技术在糖尿病相关血管并发症的价值及意义。     

血管超声对糖尿病大血管病变检测的研究进展

糖尿病（diabetes mellitus,DM）是临床常见的全身代谢性疾病,高血糖能促进血管病变而致组织器官缺血,晚期可发生多种急、慢性并发症。因此,加强对糖尿病引发的大血管病变的研究,探讨其危险因素及发病机理、寻求最恰当的诊断方法,对糖尿病患者并发脑、颈动脉及周围血管病变的预防及改善预后十分必要。糖尿病大血管病变可以通过血管超声、DSA、CT血管成像（CTA）及磁共振血管成像（MRA）等进行检查。我们仅重点就血管超声对糖尿病大血管病变的检测进行综述。     

NADPH氧化酶源性活性氧在糖尿病及其血管并发症发生中的作用机制

2型糖尿病的发病机制为胰岛素抵抗和胰岛素分泌受损.最新的研究结果显示,氧化应激在糖尿病及其并发症的发病机制中起重要作用.在高游离脂肪酸(FFA)条件下,由于活性氧(ROS)产生过多引起的氧化应激可造成胰岛素抵抗和胰岛B细胞功能丧失,导致糖尿病的发生,而血糖升高进一步加重氧化应激,引发大血管和微血管病变,产生糖尿病并发症.通过研究氧化应激在糖尿病及其并发症发病中的作用机制,为防治糖尿病及其并发症提供新的理论依据.机体内多种酶体参与了ROS的生成,如NADPH氧化酶(NOX)、黄嘌呤氧化酶、线粒体呼吸链酶复合体、内皮型一氧化氮合酶(eNOS)及脂氧合酶(LOX)等.本研究旨在探讨NOX源性ROS在糖尿病及其血管并发症发生中的作用机制.     

利拉鲁肽治疗2型糖尿病合并非酒精性脂肪性肝病的研究进展

非酒精性脂肪性肝病(NAFLD)是常见的慢性肝脏疾病,患病率逐年上升,胰岛素抵抗及氧化应激是主要发病机制,目前仍缺乏有效的治疗药物。胰岛素抵抗也是引起2型糖尿病的主要发病机制,糖尿病患者NAFLD患病率较非糖尿病患者高。利拉鲁肽是人胰高血糖素样肽1受体激动剂,可改善胰岛素抵抗,越来越多研究发现利拉鲁肽对2型糖尿病合并NAFLD有一定疗效,相关机制仍未完全明确。就利拉鲁肽治疗2型糖尿病合并NAFLD的疗效及相关机制的研究进展进行综述。     

RNA干扰技术及其在2型糖尿病中的应用

RNA干扰(RNAi)技术是基因分析和基因治疗的重要手段,它在2型糖尿病中的应用涉及功能基因组研究、2型糖尿病发病机制及其心血管并发症研究。RNAi具有高效特异性的特点。然而仍需克服如何避免RNAi衰减现象,如何合理调节多基因表达等困难。     

452例2型糖尿病患者并发症的临床分析

目的通过对452例2型糖尿病患者并发症的回顾性分析,了解糖尿病并发症发病情况及相关因素,为针对性防治措施提供科学依据.方法收取我院2002年至2003年住院病人中按WHO标准确诊为2型糖尿病的病例452例,按神经病变、糖尿病肾病、眼病、脑血管意外、心脏病及其它进行分类,再进行分析.结果单一并发症发病率最高.并发症中神经病变为最多,占43%;病程越长,平均血糖水平愈高,并发症愈多.结论糖尿病并发症与其病程,平均血糖水平相关.     

2型糖尿病合并脂肪肝患者一氧化氮水平及相关因素的研究

脂肪肝是糖尿病患者较为严重的并发症之一，确切发病机制不清，一氧化氮(NO)是一氧化氮合酶(NOS)催化L-精氨酸生成的一种小分子物质，参与扩张血管，抑制血小板聚积，抑制白细胞粘附，改善微循环。NO水平的高低反映了糖尿病患者的病情程度，及机体的抗氧化能力。我们对2型糖尿病伴脂肪肝患者血清NO及相关因素进行了系统研究，现报告如下。     

糖尿病脑病研究进展

目的糖尿病脑病是糖尿病并发症之一，以认知功能障碍为主要表现。此病的发病机制复杂，其诊断标准不明确。本文从糖尿病脑病的发病机制、病理形态改变、临床表现及与Alzheimer病、神经营养因子之间的关系等方面阐述糖尿病脑病的研究现状和进展。     

维生素D和糖尿病

维生素D最重要的功能是维持人体钙离子代谢的平衡。随着研究的深入，维生素D在炎性反应、自身免疫性疾病、胰岛素分泌及胰岛素抵抗等方面的作用已经成为研究的热点。维生素D缺乏或不足与糖尿病发病相关。维生素D可通过抑制炎性反应、促进胰岛素释放、减轻胰岛素抵抗等机制参与糖尿病的发病。大量的临床研究发现补充足量的维生素D不仅可以减少1型糖尿病和2型糖尿病的发病，而且还可以改善糖代谢，控制糖尿病相关症状。因此，维生素D可能在预防和控制糖尿病中起重要作用。     

心钠素基因多态性与2型糖尿病肾病易感性的关联研究

糖尿病肾病是 2型糖尿病的主要晚期并发症之一 ,其确切发病机制及遗传学基础尚未完全阐明。在遗传学水平早期发现糖尿病肾病高危人群 ,并对其进行积极合理的治疗可预防或延缓糖尿病肾病的发生和发展。本研究通过对 2型糖尿病正常白蛋白尿组、临床肾病组 (包括微量白蛋白尿及大量白蛋白尿 )及正常对照组之间心钠素 (ＡＮＦ)基因Ｃ/Ｔ多态性频率差异的研究 ,旨在观察ＡＮＰ基因多态性与 2型糖尿病肾病之间的关联 ,进而评估该基因多态性在 2型糖尿病肾病中的作用。一、对象和方法1.对象 :据 1985年ＷＨＯ诊断标准确诊的 2型糖尿病患者 (ＤＭ组 …     

Vascular function in Type 2 diabetes mellitus and pre-diabetes: the case for intrinsic endotheiopathy.

Diabetic angiopathy is a major cause of morbidity and mortality in Type 2 diabetes mellitus (DM). The pathogenesis of vascular complications in this condition appears to be complex, with distinct differences being observed between Type 1 and Type 2 DM. This review outlines the evidence for these differences and identifies endothelial dysfunction as an important associate and antecedent of Type 2DM, which predisposes to characteristic vascular complications and may also have implications for fetal development.     

二甲双胍:2型糖尿病治疗的基础药

糖尿病是一种临床常见多发的慢性代谢疾病，严重危害着人类健康与生命。糖尿病的药物治疗对控制血糖和延缓并发症发生十分重要，其中二甲双胍在2型糖尿病药物治疗中具有基石地位。     

表观遗传学在2型糖尿病发病及防治中的作用

2型糖尿病(T2DM)的病因和发病机制较为复杂,至今末完全明了.最新研究发现,能量代谢失调或宫内营养障碍等环境因素可以导致DNA甲基化和组蛋白修饰等表观遗传学变化,进而产生"代谢记忆",影响胰岛β细胞的发育和分泌功能,降低机体对胰岛素的敏感性等,最终导敛T2DM的发生.这些表观遗传学改变可被诸如特殊饮食、药物及生活方式重塑等方法予以纠正和逆转,这为T2DM的预防提供了新的思路,为治疗提供了潜在的药物靶点.本文就表观遗传学在T2DM发病及防治中作用的研究进展进行综述,并展单未来表观遗传学在T2DM领域的研究重点和方向.     

Metabolic syndrome as a predictor of type 2 diabetes,and its clinical interpretations and usefulness

Metabolic syndrome is defined as a cluster of glucose intolerance, hypertension, dyslipidemia and central obesity with insulin resistance as the source of pathogenesis. Although several different combinations of criteria have been used to define metabolic syndrome, a recently published consensus recommends the use of ethnic‐specific criteria, including waist circumference as an indicator of central obesity, triglyceride and high‐density lipoprotein (HDL) cholesterol as indicators of dyslipidemia, and blood pressure greater than 130/85 mmHg. The definition of dysglycemia, and whether central obesity and insulin resistance are essential components remain controversial. Regardless of the definition, the prevalence of metabolic syndrome is increasing in Western and Asian countries, particularly in developing areas undergoing rapid socioenvironmental changes. Numerous clinical trials have shown that metabolic syndrome is an important risk factor for cardiovascular disease (CVD), type 2 diabetes mellitus and all‐cause mortality. Therefore, metabolic syndrome might be useful as a practical tool to predict these two major metabolic disorders. Comprehensive management of risk factors is very important to the improvement of personal and public health. However, recent studies have focused on the role metabolic syndrome plays as a risk factor for CVD; its importance in the prediction of incident diabetes is frequently overlooked. In the present review, we summarize the known evidence supporting metabolic syndrome as a predictor for type 2 diabetes mellitus and CVD. Additionally, we suggest how metabolic syndrome might be useful in clinical practice, especially for the prediction of diabetes.     

The role of the renin angiotensin hormonal system in the metabolic syndrome and type 2 diabetes

Potentially important new findings have recently been reported concerning the so-called metabolic syndrome in relation to the renin-angiotensin system, ie, that treatment with inhibitors of the angiotensin-converting enzyme (ACE) not only decreases blood pressure levels but prevents the development of diabetes mellitus. The new findings described in this article highlight the potential role of the ACE system in the regulation of insulin sensitivity, thus contributing to the development of type 2 diabetes and metabolic syndrome. In addition to the well known selective effects of ACE inhibitors and angiotensin II receptor blockers in reducing microalbuminuria in diabetic patients, the potential ability of these drugs to reduce the risk of diabetes and the metabolic syndrome would support their use as first line agents not only in diabetic patients but also in selected groups of hypertensive patients, who are particularly at risk of developing metabolic complications. This information supports the Joint Guidelines for the Management of Arterial Hypertension by the European Society of Hypertension and the European Society of Cardiology, which highlight the crucial role of ACE inhibitors and the angiotensin II receptor blockers in preventing the development of diabetes in hypertensive patients.     

关注餐后代谢紊乱,减少动脉粥样硬化

餐后状态是指从进食到血浆葡萄糖、游离脂肪酸、氨基酸和甘油三酯等物质恢复到餐前水平的过程.糖尿病患者延迟恢复的餐后高血糖和血脂紊乱造成诸多致动脉粥样硬化的病理生理改变.餐后代谢紊乱早于空腹代谢异常,这是致大血管并发症早发的重要原因.由于餐后代谢紊乱明显影响糖尿病的预后,因此将糖尿病患者餐后血脂、血糖控制在理想范围,是糖尿病长期治疗的目标.     

Relationship of residual beta-cell function, metabolic control and chronic complications in type 2 diabetes mellitus

As the relationships between C-peptide levels and metabolic control and chronic complications are poorly known in type 2 diabetes, due to the slow decline of beta-cell function, we evaluated these associations in a cohort of type 2 diabetic patients. After excluding insulin-trated subjects, 1533 patients were divided according to their C-peptide fasting levels in quartiles. Patients within the lowest C-peptide quartile showed significantly higher duration of diabetes, prevalence of retinopathy and values of HDL-cholesterol, albumin excretion rate and HbA1c, while BMI, diastolic blood pressure, percentages of hypertension and metabolic syndrome, and values of triglycerides and uric acid were significantly higher in the highest C-peptide quartile. The associations between C-peptide and duration of diabetes, AER, HbA1c, retinopathy and the components of the metabolic syndrome remained significant, after multiple adjustments. In conclusion, these data support the hypothesis that a reduced insulin secretion is associated with a longer duration of diabetes and a greater prevalence of microvascular complications, while higher insulin levels are associated with the components of the metabolic syndrome. Received: 21 August 2000 / Accepted in revised form: 5 December 2000     

1型糖尿病免疫诊断标志物的研究进展

1型糖尿病是由胰岛β细胞自身免疫性破坏引起的一种代谢性疾病.患者体内存在多种针对胰岛细胞自身抗原的自身抗体,成为1型糖尿病的免疫诊断标记物.临床目前最为常用的是胰岛细胞抗体(ICA)、胰岛素自身抗体(IAA)、谷氨酸脱羧酶抗体(GADA)和胰岛细胞瘤相关蛋白(IA)-2抗体,此外,新近发现ZnT8A和胰岛特异性的葡萄糖-6-磷酸酶催化亚基相关蛋白抗体(IG-RPA)可能在诊断上也具有重要的价值.多种自身抗体的组合诊断具有更高的特异性和敏感性.本文针对国内外对1型糖尿病免疫诊断标记物的研究进展情况,详细分析了多种免疫诊断标志抗原的哪功能、特性及在诊断方面的意义和应用.     

What does postprandial hyperglycaemia mean?

AIMS: The potential importance of postprandial glucose (PPG) control in the development of complications in Type 2 diabetes is much debated. The recent American Diabetes Association (ADA) consensus statement discussed the role of postprandial hyperglycaemia in the pathogenesis of diabetic complications and concluded that the relationship between PPG excursions and the well-established risk factors for cardiovascular disease (CVD) should be further examined. Using the ADA statement as a starting point and including the more recent American College of Endocrinology guidelines on glycaemic control, a panel of experts in diabetes met to review the role of PPG within the context of the overall metabolic syndrome, in the development of complications in Type 2 diabetes. RESULTS: Post-prandial hyperglycaemia is a risk indicator for micro- and macrovascular complications, not only in patients with Type 2 diabetes but also in those with impaired glucose tolerance. In addition, the metabolic syndrome confers an increased risk of CVD morbidity and mortality. The debate focused on the relative contributions of postprandial hyperglycaemia, the metabolic syndrome and, in particular, raised triglyceride levels in the postprandial state, to the development of cardiovascular complications of diabetes. CONCLUSIONS: The panel recommended that in the prevention and management of microvascular complications of Type 2 diabetes, targeting both chronic and acute glucose fluctuations is necessary. Lowering the macrovascular risk also requires control of (postprandial) triglyceride levels and other components of the metabolic syndrome.