肥胖、代谢综合征与炎症

流行病学、临床及实验研究结果提示，肥胖和炎症的关系是代谢综合征共同土壤的重要组成部分。肥胖和有关的代谢病生理变化伴有慢性炎症反应，产生异常的细胞因子及激活炎症信号通路，与肥胖本身以及与其密切相关的疾病状态之间存在因果关系。肥胖时炎症反应的重要特征在于它是被启动的、最初主要位于脂肪组织，其中白色脂肪组织中的巨噬细胞和炎症相关因子基因起着重要作用。炎症指标可能用于代谢综合征的预测和诊断。对肥胖与炎症之间关系的新认识为防治代谢综合征提供了新的途径。     

肥胖、代谢综合征与炎症

流行病学、临床及实验研究结果提示,肥胖和炎症的关系是代谢综合征共同土壤的重要组成部分。肥胖和有关的代谢病生理变化伴有慢性炎症反应,产生异常的细胞因子及激活炎症信号通路,与肥胖本身以及与其密切相关的疾病状态之间存在因果关系。肥胖时炎症反应的重要特征在于它是被启动的、最初主要位于脂肪组织,其中白色脂肪组织中的巨噬细胞和炎症相关因子基因起着重要作用。炎症指标可能用于代谢综合征的预测和诊断。对肥胖与炎症之间关系的新认识为防治代谢综合征提供了新的途径。     

炎症与代谢综合征

大量的流行病学调查和实验研究结果提示代谢综合征(MS)是一个低度的系统性的炎症状态,炎症通过各种炎症机制参与了MS的发生发展。炎症机制已经成为MS发生机制中一个重要研究方向,炎症也已经成为治疗MS的可能有效靶点。     

从肥胖到慢性炎症

最近《细胞代谢》杂志的一篇报道：研究者已经发现在食谱中导致由肥胖引起慢性轻度炎症的关键成分了。     

高血压与炎症的研究进展

高血压病的发生机制是一个复杂的病理过程。其中,全身动脉血管炎症反应参与高血压的病理生理过程,它是多种炎症细胞、递质、细胞因子共同作用的结果。现综述炎性细胞、炎性细胞因子在高血压发生发展过程中的作用,并介绍高血压的抗炎治疗进展。     

脂肪细胞产物与肥胖和代谢综合征

脂肪细胞释放多种代谢产物、激素和细胞因子，与肥胖和代谢综合征的发病关系密切，其中瘦素和新近发现的脂联素更引人注目。若能对这些脂肪细胞产物趋利避害，将有可能成为治疗肥胖和代谢综合征的一个突破点。     

肠道菌群与肥胖及相关代谢紊乱疾病炎症状态关系的研究进展

目前认为肥胖以及与其相关的代谢紊乱疾病可以视为机体的一种炎症状态,而肠道菌群很可能参与此状态的发病和调节过程.此文对肠道菌群与肥胖炎症状态的关系和可能作用机制进行综述,以期寻找出能够控制肥胖的新方法.     

肥胖与免疫炎症

肥胖是一种代谢性疾病,同时也是一种慢性炎症状态.脂肪组织是炎症反应的始动环节,其中巨噬细胞发挥着促炎的重要功能,可以引起胰岛素抵抗.另外T细胞和肥大细胞也参与了脂肪组织的慢性炎症过程.     

肥胖对代谢相关脂肪性肝病血清学影响的研究进展

代谢相关脂肪性肝病(MAFLD)在全球范围内已逐渐成为最常见的肝病之一,尤其是与肥胖相关的代谢综合征人群。目前诊断MAFLD的金标准是肝活检,但存在诸多弊端,我们需要高准确性的血清学方法和评分模型来识别及评估早期肝脏病变。我国的肥胖人群以腹型肥胖为主,而肥胖会影响MAFLD人群血清标志物及评分模型,本文着重论述血清学标志物、评分模型在肥胖MAFLD人群中的影响。     

慢性炎性反应与儿童肥胖及代谢综合征

The prevalence of overweight and metabolic syndrome is increasing in young people. Body fat produces a number of inflammatory cytokines, such as C-reactive protein, TNF-α, IL-6, etc, which lead to chronic subclinical inflammation. Chronic subclinical inflammation in childhood and adolescents is as-sociated with obesity,which closely related with metabolic syndrome and insulin resistance at all ages. This feature of the diseases provides an opportunity for the early identification of target groups and the use of ap-propriate lifestyle intervention can effectively interrupt the pathological processes at early stages.     

Obesity and novel management of inflammatory bowel disease

Obesity is prevalent within the inflammatory bowel disease(IBD) population,particularly in newly developed countries.Several epidemiological studies have suggested that 15%-40% of IBD patients are obese,and there is a potential role of obesity in the pathogenesis of IBD.The dysfunction of mesenteric fat worsens the inflammatory course of Crohn’s disease and may induce formation of strictures or fistulas.Furthermore,obesity may affect the disease course or treatment response of IBD.Given the incr...     

Changes in circulating sirtuin 1 after bariatric surgery

Background and aimsObesity is associated with chronic inflammation and oxidative stress. Weight loss after bariatric surgery improves the inflammatory state and risk of cardiovascular disease. Improvement in metabolic dysfunction might be associated with changes in the activity of sirtuin 1 (SIRT1) and we aimed to investigate the effect of bariatric surgery on its circulating levels.Methods and resultsThis is a sub-study of a prospective cohort study, including 110 subjects with morbid obesity. The surgical procedure was either laparoscopic Roux-en-Y gastric bypass (RYGB) or sleeve gastrectomy (SG). Blood was sampled at inclusion and six and 12 months after surgery. SIRT1 was measured in EDTA plasma with an enzyme-linked immunosorbent assay. The mean age in the population was 43 years, 80% were women and mean body mass index (BMI) was 38.8 kg/m². RYGB and SG were performed in 89 and 21 subjects, respectively. SIRT1 concentration was significantly reduced from baseline to six and 12 months after surgery, with mean values (SD) 156.8 (82.6), 119.5 (65.6) and 94.9 (45.6) ng/mL, respectively, (p ≤ 0.002, all), accompanied by significant reductions in C-reactive protein (CRP), BMI and triglycerides from inclusion (p < 0.001, all). Type of surgery did not differently modify SIRT1 levels (p = 0.09). CRP and triglycerides were both positively predictive of SIRT1 levels (p ≤ 0.001, both).ConclusionSIRT1 concentration was significantly lower six and 12 months after bariatric surgery. CRP and triglycerides independently predicted SIRT1 levels, suggesting that reduction in SIRT1 levels might not intrinsically be related to weight reduction, but to improvement in metaflammation.     

Obesity and colorectal cancer:Role of adipokines in tumor initiation and progression

Obesity-associated diseases account for a large portion of public health challenges.Among obesity-related disorders,a direct and independent relationship has been ascertained for colorectal cancer(CRC).The evidence that adipocyte hypertrophy and excessive adipose tissue accumulation(mainly visceral)can promote pathogenic adipocyte and adipose tissue-related diseases,has led to formulate the concept of"adiposopathy",defined as adipocyte and adipose tissue dysfunction that contributes to metabolic syndrome.Adipose tissue can,indeed,be regarded as an important and highly active player of the innate immune response,in which cytokine/adipokine secretion is responsible for a paracrine loop between adipocytes and macrophages,thus contributing to the systemic chronic low-grade inflammation associated with visceral obesity,which represents a favorable niche for tumor development.The adipocyte itself participates as a central mediator of this inflammatory response in obese individuals by secreting hormones,growth factors and proinflammatory cytokines,which are of particular relevance for the pathogenesis of CRC.Among adipocyte-secreted hormones,the most relevant to colorectal tumorigenesis are adiponectin,leptin,resistin and ghrelin.All these molecules have been involved in cell growth and proliferation,as well as tumor angiogenesis and it has been demonstrated that their expression changes from normal colonic mucosa to adenoma and adenocarcinoma,suggesting their involvement in multistep colorectal carcinogenesis.These findings have led to the hypothesis that an unfavorable adipokine profile,with a reduction of those with an anti-inflammatory and anti-cancerous activity,might serve as a prognostic factor in CRC patients and that adipokines or their analogues/antagonists might become useful agents in the management or chemoprevention of CRC.     

The Impact of Obesity on Risk Factors and Prevalence and Prognosis of Coronary Heart Disease—The Obesity Paradox

Obesity is associated with a host of cardiovascular risk factors and its prevalence is rising rapidly. Despite strong evidence that obesity predisposes to the development and progression of coronary heart disease (CHD), numerous studies have shown an inverse relationship between various measures of obesity (most commonly body mass index) and outcomes in established CHD. In this article we review the evidence surrounding the ? obesity paradox ? in the secondary care of CHD patients and the CHD presentations where a paradox has been found. Finally we discuss the impact of cardiorespiratory fitness and a number of mechanisms which may offer potential explanations for this puzzling phenomenon.     

Influence of Obesity on Outcomes in Atrial Fibrillation: Yet Another Obesity Paradox

Background

Obese patients have favorable outcomes in congestive heart failure, hypertension, peripheral vascular disease, and coronary artery disease. Obesity also has been linked with increased incidence of atrial fibrillation, but its influence on outcomes in atrial fibrillation patients has not been investigated. The objective of this research is to investigate the effect of obesity on outcomes in atrial fibrillation.

Methods

The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study was one of the largest multicenter trials of atrial fibrillation, with 4060 patients. Subjects were randomized to rate versus rhythm-control strategy. We performed a post hoc analysis of the National Heart, Lung and Blood Institute limited access dataset of atrial fibrillation patients who had body mass index (BMI) data available in the AFFIRM study. BMI data were not available on 1542 patients. Patients with BMI ≥18.5 were split into normal (18.5-25), overweight (25-30), and obese (>30) categories as per BMI (kg/m²). Multivariate Cox proportional hazards regression was used on the eligible 2492 patients. End points were all-cause mortality and cardiovascular mortality.

Results

Over three fourths of all patients in our cohort were overweight or obese. There were 304 deaths (103 among normal weight, 108 among overweight, and 93 among obese) and 148 cardiovascular deaths (54 among normal weight, 41 among overweight, and 53 among obese) over a mean period of 3 years of patient follow-up. On multivariate analysis, overweight (hazard ratio [HR] 0.64; 95% confidence interval [CI], 0.48-0.84; P = .001) and obese (HR 0.80; 95% CI, 0.68-0.93; P = .005) categories were associated with lower all-cause mortality as compared with normal weight. Overweight (HR 0.40; 95% CI, 0.26-0.60; P <.001) and obese patients (HR 0.77; 95% CI, 0.62-0.95; P = .01) also had lower cardiovascular mortality as compared with the normal weight patients.

Conclusions

Although in prior studies, obesity has been associated with increased risk of atrial fibrillation, an obesity paradox exists for outcomes in atrial fibrillation. Obese patients with atrial fibrillation appear to have better long-term outcomes than nonobese patients.     

急性胰腺炎患者致炎与抗炎因子的变化及生长抑素的调节作用

目的:探讨急性胰腺炎患者血浆中致炎因子肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)和抗炎因子转化细胞生长因子-β(TGF-β)、白介素-10(IL-10)的变化、意义及生长抑素的调节作用。方法:急性胰腺炎48例,随机分成生长抑素治疗组和常规治疗组,分别在治疗前(入院时)、治疗后8 h和第2、3、4 d清晨空腹抽肘静脉血3 ml,测定TNF-α、IL-6、TGF-β和IL-10,并设对照组。结果:TNF-α和IL-6各监测点均比对照组显著升高(P<0.05,P<0.01),高峰在入院时。TGF-β和IL-10入院后8 h以后各监测点均比对照组显著升高(P<0.05,P<0.01);第2天达高峰。生长素抑素治疗组TNT-α、IL-6、和TGF-β、IL-10含量治疗后8 h明显低于常规治疗组。治疗后各观察点持续降低(P<0.05,P<0.01)。结论:急性胰腺炎患者血中致炎因子与抗炎因子均升高,机体免疫功能紊乱。生长抑素对致炎因子与抗炎因子的升高有抑制作用。     

Obesity and the Obesity Paradox in Heart Failure

Obesity is a growing public health problem in the general population, and significantly increases the risk for the development of new-onset heart failure (HF). However, in the setting of chronic HF, overweight and mild to moderate obesity is associated with substantially improved survival compared to normal-weight patients. Evidence exists for an “obesity paradox” in HF, with the majority of data measuring obesity by body mass index, but also across various less-frequently used measures of body fat (BF) and body composition including waist circumference, waist–hip ratio, skinfold estimates of percent BF, and bioelectrical impedance analysis of body composition. Other emerging areas of investigation such as the relationship of the obesity paradox to cardiorespiratory fitness are also discussed. Finally, this review explores various explanations for the obesity paradox, and summarizes the current evidence for intentional weight loss treatments for HF in context.