餐后高血糖的研究进展

餐后血糖是血糖谱的主要组成部分。餐后高血糖包括非糖尿病状态下和糖尿病状态下餐后高血糖两大类。本文就餐后高血糖的危害性及其防治简要进行介绍。     

餐后高血糖及其控制

糖尿病高血糖可有两种形式,一为空腹、餐后均有血糖升高,二为空腹血糖正常或微高而餐后血糖明显升高。由此可见,餐后高血糖是糖尿病患者的共性现象。只有血糖总体水平(包括空腹及餐后)得到良好的控制,才能有效地预防和延缓糖尿病慢性并发症的发生。而且糖血病早期往往仅有餐后血糖升高,所以重视检查餐后血糖,也是防止漏诊的重要措施。餐后2小时血糖(PBG)以控制在4.5～7.8mmol/L为最佳状态,7.9～8.9mmol/L较好。葡萄糖耐量减低(IGT)时,机体在较多时间内已超过上述水平。治疗不当的糖血病患者,进餐后高血糖状态持续的时间比空腹时正常血糖…     

关注餐后高血糖

通常体检,我们都会在之前被告知要空腹,所以一般的查体,经常都是查空腹血糖。而血糖的增高是由空腹和餐后两部分组成,早期糖尿病病人,通常是表现为空腹血糖正常,     

餐后高血糖106例与心血管疾病临床分析

对本科206例心血管疾病住院患进行空腹及餐后二小时血糖检查，采用美国ONE—TOUCH血糖仪测定，结果检出餐后血糖升高106例，占51．46％，空腹血糖升高35例，占16．99％，空腹和餐后血糖均升高8例，占3．88％。结论：餐后二小时血糖升高检出率与心血管病关系密切，应引起高度重视，需采取相应的预防措施。     

降低餐后高血糖新策略

中华医学会学术推广部经国际糖尿病联盟(IDF)正式授权,于2007年3月6～9日分别在北京、杭州、上海、广州等4个城市召开“IDF中国区论坛——降低餐后高血糖新策略”学术研讨会。我国医生与IDF专家John Turtle、John Turtle、Clive Cockram就降低餐后血糖的一些热点问题进行了交流,现摘录如下。问:IDF有没有一个专门针对餐后高血糖的治疗指南?答:IDF已经认识到降低餐后高血糖在控制2型糖尿病患者的血糖和心血管并发症中的重要性。现正制定关于餐后高血糖控制的指南,在未来的几个月内将会向大家公布。问:为什么提出通过恢复胰岛素早期…     

餐后高血糖危害大

继10年前国内学者认识到餐后高血糖的危害，糖尿病治疗在强调控制空腹血糖的同时，越来越重视餐后血糖的达标。虽然控制空腹高血糖非常必要，但离达到理想的血糖控制还常常不够。越来越多的证据显示减少餐后血糖波动对糖化血红蛋白达标（我国规定小于6．5％）同等重要，甚至可能更加重要。     

三原则控制餐后高血糖

刚得病时,每天的任务就是忙于控制空腹血糖,可一段时间之后,我发现餐后血糖也居高不下,慌乱中,经人介绍我结识了《糖尿病之友》,在她的帮助下,我努力改变,将知识与实践相结合,我成功了。     

餐后高血糖该如何应对

有位王先生，48岁，近来体检，发现了糖尿病。他在医院诊治，空腹血糖能控制到6毫摩尔／升（mmol／L）左右。有次看到本刊一篇关于测餐后血糖比空腹血糖更重要的文章，就去测了一次餐后2小时血糖，竞达到12mmol／L，大吃一惊。那么餐后血糖升高到底代表着什么，又有哪些危害，我们该如何防治餐后高血糖这个隐形杀手呢？     

餐后高血糖与心血管疾病

近年来研究表明，餐后高血糖与心血管疾病的发生有着密切的关系。胰岛素急性分泌受损、胰岛素抵抗是餐后高血糖的原因。餐后高血糖是心血管疾病发病的独立危险因素，对于预测心血管疾病的发生有重要的价值。积极干预餐后高血糖可明显减少心血管疾病的发病率和病死率。餐后高血糖可使蛋白质等非酶糖基化过程加快，山梨醇途径活跃，自由基生成增加，促使动脉粥样硬化的过程明显加快，从而导致心血管疾病。     

餐后高血糖与心血管疾病

近年来研究表明,餐后高血糖与心血管疾病的发生有着密切的关系.胰岛素急性分泌受损、胰岛素抵抗是餐后高血糖的原因.餐后高血糖是心血管疾病发病的独立危险因素,对于预测心血管疾病的发生有重要的价值.积极干预餐后高血糖可明显减少心血管疾病的发病率和病死率.餐后高血糖可使蛋白质等非酶糖基化过程加快,山梨醇途径活跃,自由基生成增加,促使动脉粥样硬化的过程明显加快,从而导致心血管疾病.     

餐后高血糖与脑血管病

餐后血糖升高是动脉粥样硬化和脑血管病的危险因素.文章分别从餐后高血糖参与动脉粥样硬化的病理生理学机制、餐后高血糖与脑血管病的关系及其病理生理学机制等方面,综述了餐后高血糖引起脑血管病的机制.     

Postprandial hyperglycemia

Chronic hyperglycaemia, confirmed with HbA1c levels, is a leading cause of diabetic complications. Recent studies point to a significant effect of postprandial glycaemia which results from an impaired ability of early secretion of insulin in type II diabetes. Postprandial hyperglycaemia is a frequent phenomenon in people with diabetes with satisfactory control of diabetes based on checks of HbA1c levels. Many authors demonstrate statistically more significant correlations between postprandial hyperglycaemia and HbA1c levels, compared to correlation of fasting glycaemia. Monitoring of postprandial glycaemia is a significant means for improving co-operation with a patient and provides a physician with a possibility of choice between an appropriate type of peroral antidiabetic or insulin.     

餐后血糖调节与糖尿病心血管疾病并发症

如何确定餐后高血糖水平及其与糖化血红蛋白(Hb)A1c的相关性,近年来研究结果不一致。虽然高血糖在糖尿病并发症发生、发展中的直接作用目前仍有争议,但众多流行病学研究已证实,与HbA1c相比,餐后血糖是一个更好的预测心血管疾病危险性的因素。其致病机制与氧化应激对血管内皮的毒性作用及其对总体血糖的贡献有关。目前的观点普遍认为,控制餐后血糖是预防与糖尿病相关的心血管疾病并发症的一项重要的策略。     

Postprandial hyperglycemia/hyperlipidemia (postprandial dysmetabolism) is a cardiovascular risk factor

Epidemiologic data indicate that a postprandial state characterized by abnormally increased levels of glucose and lipids (also referred to as postprandial dysmetabolism) is an independent predictor of future cardiovascular events, even in nondiabetic subjects. The cardiovascular toxicity of postprandial dysmetabolism is mediated by oxidant stress, which is directly proportional to the increase in glucose after a meal. This transient increase in free radicals acutely triggers inflammation, endothelial dysfunction, hypercoagulability, sympathetic hyperactivity, and a cascade of other atherogenic changes. The postprandial dysmetabolism hypothesis has been bolstered by interventional studies that have demonstrated that blunting the postprandial spikes in glucose and lipids improves inflammation and endothelial function immediately. Early randomized controlled trials indicate that reducing postprandial dysmetabolism appears to significantly slow atherosclerotic progression and may improve cardiovascular prognosis. In conclusion, postprandial dysmetabolism appears to be an important proximate cause of adverse cardiovascular events. Addressing this fundamental and largely unrecognized condition will require specific screening and treatment strategies. Diet, exercise, and various pharmacologic agents can improve postprandial dysmetabolism. Using these strategies may help improve the prognosis for patients with diabetes mellitus and/or coronary heart disease.     

Postprandial lipemia and cardiovascular disease

Postprandial lipemia, characterized by a rise in triglyceride-rich lipoproteins after eating, is a dynamic, nonsteady-state condition in which humans spend the majority of time. There are several lines of evidence suggesting that postprandial lipemia increases risk of atherogenesis. Clinical data show a correlation between postprandial lipoproteins and the presence/progression of coronary artery disease and carotid intimal thickness. Mechanistic studies demonstrate that triglyceride-rich lipoprotein remnants may have adverse effects on endothelium and can penetrate into the subendothelial space. Exchange of core lipids between postprandial lipoproteins and low-density lipoprotein (LDL)/high-density lipoprotein (HDL) is increased during prolonged lipemia, resulting in small, dense LDL particles and reduced HDL cholesterol levels. Hemostatic variables, including clotting factors, platelet reactivity, and monocyte cytokine expression, may be increased during postprandial lipemia. Collectively, these data suggest that assessment and treatment of atherosclerosis should include parameters related to postprandial lipemia.     

Postprandial lipid oxidation and cardiovascular disease risk

A mild pro-oxidative state accompanies meal ingestion, which results in an increase in biomarkers of inflammation, adhesion, and endothelial dysfunction, all of which are factors in the development of cardiovascular disease. Both fat and carbohydrate can cause the effect, which is additive and exacerbated by diabetes. The presence of lipid, glucose, and cholesterol oxidation products of dietary or endogenous origin may contribute to postprandial oxidative stress. However, the generation of excess superoxide due to abundant energy substrate after the meal may be a predominate factor resulting in oxidative stress and a decrease in nitric oxide, which is important to endothelial function. Remediation of postprandial oxidative stress through direct reduction of superoxide generation and simultaneous consumption of antioxidants with each meal should be a focus of future research.     

Postprandial lipemia, diet, and cardiovascular risk

Recently published studies have provided additional evidence of the pathophysiology and clinical relevance of postprandial dyslipidemia. Notably, the relationship with cardiovascular risk has been considerably strengthened by two large prospective studies showing an independent role for nonfasting plasma triglycerides. Knowledge of the genetic influence has been expanded by the identification of new gene variants associated with postprandial lipemia. More data have confirmed the strict relation between postprandial lipoprotein alterations and insulin resistance, whereas studies on the association with endothelial dysfunction have not been conclusive. Recent medium-term intervention studies have mainly evaluated the different dietary fatty acids and compared diets rich in monounsaturated fatty acids with diets rich in carbohydrates. Results indicate that the diet generally recommended for cardiovascular prevention (ie, low in saturated fat, rich in omega-3 fatty acids, moderately rich in carbohydrates, and rich in fiber) may also correct postprandial lipid abnormalities.     

Postprandial glycemia and cardiovascular disease in diabetes mellitus

This article reviews the role of fasting and postprandial glycemia to the overall glycemic control of patients with type 2 diabetes and glucose intolerance, as well as their causal relationship upon micro and macrovascular complications. Recent studies have suggested that a third component of the glucose triad, the postprandial glucose excursions, might have a role in the overall glycemic load and might also reflect glycemic control. Epidemiological and intervention studies are presented in the article, supporting the conclusion that postprandial hyperglycemia in impaired glucose tolerance and diabetic subjects is a more powerful marker of cardiovascular disease risk than fasting hyperglycemia, then the treatment directed at specifically lowering postprandial glucose is crucial, as underlined by the American Diabetes Association.