血清瘦素与肥胖性高血压及动脉顺应性的关系

瘦素是由肥胖基因编码的一种蛋白质，在心血管疾病中起着重要作用，已成为近年来国内外多学科共同研究的热点。本研究旨在探讨在江苏省南京市部分汉族人群中血清瘦素与高血压、肥胖及动脉顺应性的关系，为心血管疾病的防治开辟新的途径。     

体重与心血管疾病死亡的关系

随着全球超重/肥胖患病率的上升和研究的累积,人们逐渐认识到超重/肥胖在心血管疾病及死亡中发挥的重要作用。本文从超重/肥胖的诊断及分级出发,通过回顾流行病学证据,初步探讨了其导致心血管疾病及死亡的可能机制,并围绕体重与心血管结局之间的关系展开论述。此外,对于体重的管理,除了生活方式及药物干预之外,尤其应关注降糖药物对糖尿病患者体重的不同影响。     

肥胖与心血管疾病相关性的研究进展

肥胖是心血管疾病的独立危险因素。然而有研究表明,与心血管疾病患者中体质量正常或偏低者相比,肥胖者的预后较好,这种现象被称为"肥胖矛盾"。该文介绍近年来有关肥胖与心血管疾病关系的研究进展。     

肥胖与糖尿病及心血管事件:流行现状及研究新进展

心血管疾病死亡目前已位居全死因顺位的第一位,其中约80％发生在中、低收入国家.心血管疾病是多种危险因素如糖尿病或糖调节异常、肥胖、血脂紊乱、高血压以及生活方式、饮食习惯、遗传因素等相互作用和累加的结果,其中超重和肥胖是心血管疾病的重要危险因素.然而研究表明,肥胖与心血管疾病之间的联系不仅取决于总体脂量,而且与脂肪组织的分布异常有密切关系,其中最值得关注的是腹部脂肪聚积在糖尿病及心血管疾病的发生和发展过程中所起的作用[1].     

代谢综合征研究进展

代谢综合征是近年来研究的热点问题。高血压、血脂异常、糖耐量减退和肥胖常同时发生，与心血管疾病关系密切。本文就其意义、发病机制和防治方法做一综述。     

儿童期肥胖、成年期肥胖和心血管风险因子

过去30年,儿童超重或肥胖的发生率明显增加[1]。儿童期肥胖是死亡率增加的预测因子,这主要是由于儿童期肥胖可导致心血管疾病发生率增加。相关的预测研究提示"肥胖流行症"可能改变目前心血管疾病死亡率下降的趋势,使现今儿童的寿命缩短。有足够的证据表明肥胖与心血管疾病之间有相关性是由     

Resistin在脂肪与胰岛素抵抗之间的作用

以胰岛素抵抗为特征的 2型糖尿病正成为全球关注的健康问题 ,而疾病流行调查表明 ,2型糖尿病肥胖患者的比例超过80 % ,这说明胰岛素抵抗与肥胖即脂肪细胞之间具有密切的关系。与肥胖相关的胰岛素抵抗不仅表现为 2型糖尿病 ,还有脂质代谢紊乱、异常高血凝状态及心血管疾病等[1 ] 。在探讨肥胖与胰岛素抵抗之间关系的研究中 ,Steppan等[1 ] 发现一种新的由脂肪细胞分泌的蛋白 ,他们称之为 Resistin(抗素 ) ,意为引起胰岛素抵抗的物质 (也有称之为 Fizz3)。随后围绕 Resistin进行了一系列研究 ,本文将研究的结果综述如下。一、Resistin的发现…     

肥胖发病机制的研究进展

肥胖是环境因素和遗传因素之间经过复杂的相互作用所致的代谢综合征。肥胖能够引起全身的能量代谢发生紊乱,大大增加高血压、冠心病等心血管疾病的发病风险。肥胖发病涉及多个复杂系统以及他们之间的相互作用。正确认识肥胖的发病机制是指导制定肥胖预防和治疗策略的前提。目前对肥胖发病的分子机制的研究逐步深入,本文系统总结近年来对肥胖发病机制的研究进展。     

肥胖矛盾现象

肥胖是目前全球面临的重大公共卫生问题之一.肥胖既是多种心血管疾病与代谢病的主要危险因素,也是重要的致病因子.但是,近年来,一些横断面分析和回顾性研究发现,体质指数与心血管预后及靶器官损害呈负相关,有学者将这种现象称为＂肥胖矛盾＂.     

胰高血糖素样肽-1受体激动剂治疗肥胖性心肌病作用机制的研究进展

肥胖是心血管疾病的重要独立危险因素,可增加心血管疾病的风险,长期肥胖可引起心脏功能紊乱,发展为肥胖性心肌病,严重者可导致心力衰竭,研究更安全有效的肥胖性心肌病治疗方法迫在眉睫。近年来基于肥胖人群的研究表明,GLP-1 RA可有效降低肥胖患者心血管疾病发病的风险,可能通过抗氧化应激、抑制炎性反应、改善微循环功能障碍以及抵制心肌纤维化等多个方面发挥作用。     

中心性肥胖的糖耐量低减患者的临床特点分析

目的探讨中心性肥胖的糖耐量低减（IGT）患者的临床特点及防治策略。方法将IGT患者69例分为中心性肥胖组（试验组）31例，非中心性肥胖组（对照组）38例，比较其体重指数、收缩压和脉压、血脂异常和心血管病发病率、饮食和运动习惯等的差异。结果合并中心性肥胖的IGT患者超重和肥胖率、非HDL-C性高脂血症的发生率、饮食和运动习惯的良好率与对照组相比差异有显著性。收缩压和脉压、心血管病的发生率与对照组相比差异无显著性。结论合并中心性肥胖的IGT患者肥胖、高脂血症的发病率更高，胰岛素抵抗更严重，应从饮食和运动习惯人手积极干预，预防糖尿病及其血管病变的发生。     

Philosophical determinants of obesity as a disease

Is obesity a disease? Much ink has been spilled over this debate and for good reasons. The global prevalence of obesity has more than doubled since the 1980s and is now of pandemic proportions. Whether obesity is a disease has consequences for what kind of treatments are appropriate, as well as how we ought to allocate funding and access to healthcare resources. In most cases, there is no dispute over the medical facts, yet disagreement persists. This is because whether obesity is a disease is not determined by medical facts alone; the issue is, in part, conceptual. Science relies on careful argumentation and conceptual analysis as part of its armamentarium. In this review, we will examine the two concepts of disease most often employed in the philosophy of medicine: the naturalistic and constructivist. We will argue that, whichever definition of a disease is used, obesity fits the criteria for disease definition. Those seeking to meet the challenge of managing obesity will, therefore, need to embrace chronic disease models of care suited to addressing the lifelong challenge posed by this disease and its associated complications.     

Non‐nutrient causes of low‐grade,systemic inflammation: support for a ‘canary in the mineshaft’ view of obesity in chronic disease

A form of low‐grade, systemic inflammation (‘metaflammation’) is linked to many types of chronic disease. Initially, this was thought to be causally related to weight gain and obesity and a possible explanation of the link between obesity and disease. However, several lifestyle‐related inducers of such inflammation, some of which are associated with obesity, but some of which are not, have now been identified. The most common of these have been nutritive related, suggesting that there could still be a relationship, either directly or indirectly, with obesity. Here we provide evidence for non‐nutritive inflammatory inducers, providing further support for an earlier suggestion that while obesity, beyond a point, may have a direct link with disease, this may be neither necessary nor sufficient to explain the current epidemic of chronic disease. A more ubiquitous cause encompassing all inflammatory inducers is the modern, post‐industrial environment and lifestyles emanating from this. Obesity may thus be more of ‘a canary in the mineshaft’, warning of bigger global problems, than just a single pathway to modern environmentally driven disease.     

Tumours of kidneys, urinary bladder and prostate in obesity and diabetes

Relations of obesity and type 2 diabetes to urinary tract cancer were described. Occurrence of kidney cancer is more often in both obesity and type 2 diabetes. Bladder cancer has no relation to obesity but is more common in type 2 diabetic patients. Inverted relations were found in prostatic cancer. This disease is more common in obese patents but less common in type 2 diabetes. Diabetics are partly protected to this disease. Physical activity decreases the risk of kidney and bladder cancer but has no relation to bladder cancer. Urinary tract cancers have no relation to type 1 diabetes. We have found 3.9 time higher risk of kidney cancer in Czech diabetic patients.     

Update: systemic diseases and the cardiovascular system (i): obesity and the heart

Excess weight is the most prevalent cardiovascular risk factor and certainly the factor that improves the least over time among those with established cardiovascular disease. The association between obesity and cardiovascular disease is complex and not limited to the standard risk factors like hypertension, dyslipidemia, and type 2 diabetes mellitus. In recent years, multiple studies have shown that obesity may cause cardiovascular diseases via multiple disease mechanisms like subclinical inflammation, endothelial dysfunction, increased sympathetic tone, atherogenic lipid profiles, enhanced thrombogenic factors and also through obstructive sleep apnea.Despite the overwhelming data linking obesity to cardiovascular disease, several studies have shown a paradoxical association between obesity and prognosis among those with coronary disease and heart failure, which may be due to limitations of the way we currently define obesity. There is abundant data suggesting that measuring central obesity or total body fat content might be more appropriate than using the body mass index alone.The management of obesity is challenging and studies using lifestyle modification alone or with pharmacologic agents generally have limited success and high levels of weight regain. Bariatric surgery has proven to be an effective and safe way to induce and maintain significant weight loss but is limited to those with medically complicated obesity or people who are severely obese.Full English text available from: www.revespcardiol.org     

Should obesity be the main game? Or do we need an environmental makeover to combat the inflammatory and chronic disease epidemics?

There is a link between obesity and chronic disease. However, the causal relationship is complicated. Some forms of obesity are associated with low-level systemic inflammation, which is linked to disease. But lifestyle behaviours that may not necessarily cause obesity (poor diet, inadequate sleep, smoking, etc.) can independently cause inflammation and consequent disease. It is proposed here that it is the environment driving modern lifestyles, which is the true cause of much chronic disease, rather than obesity per se , and that obesity may be a marker of environmental derangement, rather than the primary cause of the problem. Attempts to clinically manage obesity alone on a large scale are therefore unlikely to be successful at the population level without significant lifestyle or environmental change. Environmental factors influencing obesity and health have now also been implicated in ecological perturbations such as climate change, through the shift to positive energy balance in humans caused by the exponential use of fossil fuels in such areas as transport, and consequent rises in carbon emissions into the atmosphere. It is proposed therefore that a more policy-based approach to dealing with obesity, which attacks the common causes of both biological and ecological 'dis-ease', could have positive effects on both chronic disease and environmental problems. A plea is thus made for a greater health input into discussions on environmental regulation for chronic disease control, as well as climate change.     

巨噬细胞极化与肥胖型哮喘

肥胖和支气管哮喘(简称哮喘)之间的相关性日益受到关注,大量研究证明两者之间存在关联,但是其机制尚不明确.肥胖导致机体产生的慢性低度炎症,可能是解释肥胖和哮喘关联性的因素之一.研究证明,脂肪组织中浸润的免疫细胞和炎症细胞,释放细胞因子,诱发炎症反应,损害肺、肝、心脏等其他终末器官,并引发慢性疾病如哮喘、脂肪肝、冠心病等.其中,巨噬细胞是比较重要的免疫细胞.通过巨噬细胞介导的炎症反应解释肥胖与哮喘之间的关系不容忽视.本文就巨噬细胞及其亚型特点作一综述,并阐述其与肥胖和哮喘的关联.     

Burden of disease attributable to obesity and overweight in Korea

OBJECTIVE: To estimate the burden of disease attributable to overweight and obesity using disability-adjusted life-year (DALY) in Korea. RESEARCH METHODS: Firstly, overweight and obesity-related diseases and their relative risk (RR) were selected by the systematic review. Secondly, population-attributable fractions (PAFs) were computed by using the formula including RR and the prevalence of exposure (Pe) of overweight and obesity. Thirdly, DALYs of overweight and obesity-related diseases in Korea were estimated. Finally, the attributable burden (AB) of diseases due to overweight and obesity was calculated as the sum of the products from multiplying DALYs of overweight and obesity-related diseases by their PAFs. RESULTS: The disease burden attributable to overweight was 827.1 person years (PYs) overall, 732.6 for men, 922.9 for women per 100,000 persons. The disease burden attributable to obesity was 260.0 PYs overall, 144.2 for men, 377.3 for women. Diabetes attributable to overweight and obesity accounts for highest burden among other diseases in both genders. The disease burden attributable to overweight was 3.2 times higher than that attributable to obesity. CONCLUSION: Most proportion of disease burden attributable to high body mass index (BMI) occurred among those with only moderately raised levels such as overweight, not the extremes such as obesity. It suggests that population-based, public health intervention rather than high-risk group-focused strategies are more effective to reduce the burden of disease attributable to overweight and obesity in Korea.     

Obesity, hypertension, and vascular disease

Obesity, hypertension, and related metabolic and hemodynamic abnormalities contribute significantly to cardiovascular disease in westernized societies such as the United States. Both obesity and hypertension are more prevalent among minorities such as black and Hispanic populations. Obesity substantially increases the likelihood of hypertension, and weight reduction has been shown to be an effective hygienic measure in reducing blood pressure. There is accumulating evidence that central obesity, particularly obesity that is distributed in the paraomental (visceral) region, especially predisposes one to hypertension and related metabolic abnormalities that contribute cerebrovascular disease.     

Drug Mechanisms to Help in Managing Resistant Hypertension in Obesity

Obesity is a major risk factor for the development of hypertension. Because the prevalence of obesity is increasing worldwide, the prevalence of obesity hypertension is also increasing. Importantly, hypertension in obesity is commonly complicated by dyslipidemia and type 2 diabetes mellitus and hence imposes a high cardiovascular disease risk. Furthermore, obesity is strongly associated with resistant hypertension. Activation of the sympathetic nervous system and the renin-angiotensin system, leading to renal sodium and water retention, links obesity with hypertension. There is also evidence for the release of factors by visceral adipose tissue promoting excessive aldosterone production, and a more central role of aldosterone in obesity hypertension is emerging. Randomized studies evaluating the effect of different classes of antihypertensive agents in obesity hypertension are scarce, short-lasting, and small. Considering the emerging role of aldosterone in the pathogenesis of obesity hypertension, mineralocorticoid receptor antagonism may play a more central role in the pharmacologic treatment of obesity hypertension in the near future.