肥胖与慢性炎症

肥胖及其相关的代谢类疾病严重影响人类的健康,而肥胖诱导的慢性炎症是胰岛素抵抗和代谢综合症发病的关键因素.脂肪组织慢性炎症发生的机制及其与代谢综合症的关系已经成为全球瞩目的研究热点.慢性炎症的特征主要包括脂肪组织中促炎细胞因子表达量增加,抗炎细胞因子表达量降低以及大量巨噬细胞浸润.鉴于肥胖及其相关代谢综合症对人类健康的巨大危害,现对慢性炎症的发生机制,肥胖和慢性炎症之间的关系,脂肪组织炎症中巨噬细胞浸润以及和信号传导通路进行综述.     

脂肪组织氧化应激与运动干预

脂肪组织在调控代谢稳态和运动适应中扮演着重要的角色。肥胖引起的脂肪组织氧化应激是2型糖尿病与代谢综合征等的重要病理特征,是促进脂肪组织炎症和胰岛素抵抗的重要机制。氧化应激可以引起脂肪细胞趋化因子表达,募集炎症细胞浸润脂肪组织,炎症细胞分泌大量的炎症因子,并促进了局部和系统的胰岛素抵抗与慢性炎症。运动对肥胖相关的慢性代谢病的有效干预与运动的抗氧化效应相关。本文总结了氧化应激在脂肪组织炎症和胰岛素抵抗中的作用,以及运动对脂肪组织氧化应激的调控。     

运动干预对肥胖机体体内瘦素等脂肪细胞因子作用的影响

肥胖是近年主要的流行病之一,是危害健康的全球公共卫生问题。肥胖是一种慢性低度全身性炎症,伴随着一些炎性细胞的浸润和改变,并存在脂肪细胞因子分泌紊乱。瘦素是由白色脂肪细胞分泌的一种蛋白类激素,也是促炎细胞因子,在调控体内能量与代谢等方面发挥重要作用。运动干预会使肥胖机体体内促炎因子(瘦素、TNF-α、IL-6)水平含量降低,抗炎因子(脂联素)水平含量升高。运动能够延缓肥胖机体体内炎症反应的发生。本文以体内瘦素的生理功能及作用机制为中心,系统综述了运动对肥胖性慢性炎症的调节,主要包括脂肪细胞因子瘦素、脂联素、IL-6、TNF-α,以此探讨运动干预减重降脂和减轻慢性炎症反应的机制,为防治慢性代谢性疾病提供新视角。     

肠道菌群影响宿主肥胖的研究进展

越来越多的研究结果表明,肠道菌群与宿主消化、呼吸、内分泌、心血管、神经等系统发生的疾病密切相关。目前,全世界患肥胖和Ⅱ型糖尿病的人逐渐增多。肠道菌群的平衡有利于维持宿主正常的能量代谢过程,而肠道菌群失调使机体产生慢性炎症反应及胰岛素抵抗,从而导致肥胖和Ⅱ型糖尿病等代谢性疾病的发生。本文综述了肠道菌群影响肥胖的机制,以及通过调控肠道菌群改善肥胖的方法。     

炎症因子chemerin在肥胖及其相关疾病中的作用及运动对chemerin调控的研究进展北大核心CSCD

作为一个脂肪和炎症因子,chemerin与肥胖及其相关疾病如2型糖尿病、代谢综合征、动脉粥样硬化等疾病的发生和严重程度密切相关。运动是防治肥胖及其相关疾病、改善其紊乱的糖脂代谢的有效方法;该作用与运动通过过氧化物增殖因子活化受体(PPARγ)的激活来降低肥胖及其相关疾病的血清、脂肪、肝和骨骼肌的chemerin水平有关。chemerin的降低一方面减轻炎症,另一方面改善糖脂代谢,从而防治肥胖及其相关疾病。本文就chemerin概况、其在肥胖及其相关疾病中的作用,以及运动对chemerin的调控及机制做一综述。     

肥胖微环境促进脂肪纤维化的发病机制研究进展

现代研究发现脂肪组织的功能不仅仅只是储存以及释放脂类,还作为人体的内分泌腺,在维持机体代谢平衡方面具有重要的作用。而肥胖状态时脂肪组织的分泌功能紊乱,炎症因子与脂肪因子分泌失衡,打破了机体的代谢平衡。更糟糕的是,脂肪组织形成慢性低度炎症以及缺氧微环境,引起胶原的异常沉积,脂肪组织纤维化,从而破坏脂肪组织正常功能,可能进一步导致糖尿病以及肿瘤的产生。因此,本文主要概述肥胖引起的慢性炎症和缺氧微环境通过分泌炎症因子、上调缺氧诱导因子的表达,进而改变脂肪细胞外基质的组成,最终促进脂肪纤维化的发生的机制。     

雄激素及其受体在肥胖、肥胖相关疾病及糖脂代谢紊乱中的作用

雄激素在肥胖及肥胖相关疾病如糖尿病、代谢综合征、动脉粥样硬化、高血压、心血管疾病等的发生及肥胖的糖脂代谢紊乱中的作用受到越来越多的关注。雄激素的作用主要通过雄激素受体(androgen receptor,AR)介导,AR属于核受体超家族成员,在骨骼肌、肝脏、脂肪、脑等组织中均有分布和表达。低水平的睾酮和AR功能缺失能促进肥胖及其相关疾病的发生,诱导糖脂代谢的紊乱。睾酮/AR能调控几乎所有与糖脂代谢、肥胖相关疾病发生有关的途径,包括糖脂代谢关键酶和关键蛋白、核转录因子(PPARγ、LXRα、FoxO1)、炎症反应、下丘脑的瘦素敏感性、脂肪细胞的增殖和分化、线粒体功能和血管内皮细胞功能。此外,与男性不同,高水平雄激素的女性可出现肥胖及糖脂代谢的紊乱,其机制还不清楚。本文主要就雄激素和AR在男性肥胖及其相关疾病的发生以及糖脂代谢紊乱中的作用及机制作一综述。     

炎症因子chemerin在肥胖及其相关疾病中的作用及运动对chemerin调控的研究进展

作为一个脂肪和炎症因子,chemerin与肥胖及其相关疾病如2型糖尿病、代谢综合征、动脉粥样硬化等疾病的发生和严重程度密切相关。运动是防治肥胖及其相关疾病、改善其紊乱的糖脂代谢的有效方法;该作用与运动通过过氧化物增殖因子活化受体(PPARγ)的激活来降低肥胖及其相关疾病的血清、脂肪、肝和骨骼肌的chemerin水平有关。chemerin的降低一方面减轻炎症,另一方面改善糖脂代谢,从而防治肥胖及其相关疾病。本文就chemerin概况、其在肥胖及其相关疾病中的作用,以及运动对chemerin的调控及机制做一综述。     

脂肪细胞与免疫细胞在脂肪组织炎症与代谢失调中的作用

肥胖和超重的患病率继续上升,发病率和死亡率日益增长,是造成高血压、高脂血症、动脉粥样硬化、2型糖尿病等疾病的关键因素之一。目前,针对肥胖的研究已经深入到分子层面。结果提示,肥胖状态下内脏脂肪组织中的低度、慢性炎症反应被认为是其导致胰岛素抵抗的重要病理生理机制。这篇评论的目的是总结目前先天性免疫细胞和适应性免疫细胞在脂肪组织炎症和免疫细胞失调在肥胖和胰岛素抵抗中的作用,认识免疫炎症与代谢之间关系可能为临床治疗肥胖提供靶向。     

人体脂肪组织部位差异性与代谢综合征

肥胖主要表现为脂肪组织的过度聚集,而内脏脂肪组织的集聚与代谢综合征密切相关。不同部位脂肪组织在解剖学、脂肪细胞生物学、糖脂代谢和内分泌调节上存在显著差异。与皮下脂肪组织相比,内脏脂肪组织具有较强的代谢活性,产生大量游离脂肪酸、脂肪细胞因子、激素、炎症介质等直接进入肝脏及全身组织,这些特征可能是内脏性肥胖导致胰岛素抵抗、2型糖尿病、非酒精性脂肪肝、血脂紊乱等代谢综合征的重要机制,内脏脂肪组织成为临床监测、干预和治疗的靶标。     

Molecular approach for development of new medicaments for chronic infections treatment

Owing to the progress in cellular microbiology it has been evidently proved that inflammation induced by infectious agents forms the basis of many chronic conditions. Therefore a microbial infection can be considered as a triggering factor of such widespread and significant diseases as infertility, arthritis, atherosclerosis, asthma, gastritis, stomach ulcer and cancer, neurological syndromes and some oncological formations. Practically all pathogenic and conditionally pathogenic bacteria can induce chronic infections of different organs and tissues. It has been revealed that in spite of differences of clinical syndromes and participation of different bacteria in their induction the several general mechanisms of chronic infections are detected. Failure in chronic infections therapy is due to the absence of medicaments to eradicate persistent forms of pathogens. The development of new medicaments for chronic infections treatment should be based on the selection of new specific targets, influence on which would to inhibit the mechanism of chronic infections induction.     

Mice with experimental colitis show an altered metabolism with decreased metabolic rate

Patients with inflammatory bowel disease (IBD) suffer from body weight loss, malnutrition, and several other metabolic alterations affecting their quality of life. The aim of this study was to investigate the metabolic changes that may occur during acute and chronic colonic inflammation induced by dextran sulfate sodium (DSS) in mice. Clinical symptoms and inflammatory markers revealed the presence of an ongoing inflammatory response in the DSS-treated mice. Mice with acute inflammation had decreased body weight, respiratory exchange ratios (RER), food intake, and body fat content. Mice with chronic inflammation had decreased nutrient uptake, body fat content, locomotor activity, metabolic rates, and bone mineral density. Despite this, the body weight, food and water intake, lean mass, and RER of these mice returned to values similar to those in healthy controls. Thus, murine experimental colitis is associated with significant metabolic alterations similar to IBD patients. Our data show that the metabolic responses during acute and chronic inflammation are different, although the metabolic rate is reduced in both phases. These observations suggest compensatory metabolic alterations in chronic colitis resulting in a healthy appearance despite gross colon pathology.     

固有淋巴细胞在脂质代谢中的研究进展

由于世界范围内营养条件和生活方式的变化,肥胖及其相关的代谢性疾病已成为当前威胁人类健康的重要因素之一.在能量摄取和消耗以及体内脂肪储存、分解和脂肪组织重塑的研究中,人们逐渐认识到脂质过量及异位堆积将导致代谢组织处于慢性炎症状态,这开启了肥胖相关组织炎症研究的新方向.固有淋巴细胞(innate lymphoid cell...     

Low-grade inflammation and the metabolic syndrome in children and adolescents

PURPOSE OF REVIEW: The prevalence of overweight and the metabolic syndrome is increasing in young people. This review aims to summarize current research in children and adolescents on inflammatory markers related to components of the metabolic syndrome. RECENT FINDINGS: Obesity is characterized by a state of low-grade inflammation at all ages. Body fat has been shown to correlate with the various components of the metabolic syndrome. There is evidence to show that chronic subclinical inflammation in childhood and adolescence is associated with metabolic dysfunction, which can lead to insulin resistance and the metabolic syndrome. SUMMARY: The results presented in this review highlight the underlying inflammatory mechanisms of the early stages of metabolic disorders related to obesity. The preclinical phases of diabetes and cardiovascular disease last many decades, and this feature of the diseases provides an opportunity for the early identification of target groups and the use of appropriate prevention strategies while the pathological processes are still completely reversible.     

肥胖诱发胰岛素抵抗的炎性机制

肥胖可诱发一系列慢性代谢性疾病,如2型糖尿病、血脂障碍、高血压和非酒精性脂肪肝等.这些疾病构成了当今世界人类健康的极大威胁.胰岛素抵抗是这些疾病的共有特征.胰岛素抵抗的发生与慢性低度系统炎性密切相关,涉及多条炎性信号通路的激活和胰岛素信号转导的缺陷.本文综述了肥胖、炎性与胰岛素抵抗之间的本质联系,以及肥胖诱发胰岛素抵抗的炎性机制,以期为肥胖相关疾病的防治提供重要参考.     

Mediterranean diet and metabolic diseases

PURPOSE OF REVIEW: The objective of this article is to present evidence illustrating the relationship between Mediterranean diets and metabolic diseases, including obesity, type 2 diabetes, and the metabolic syndrome, and to briefly discuss potential mechanisms by which these diets can help in disease prevention and treatment. RECENT FINDINGS: Although the Mediterranean diet has long been celebrated for its impact on cardiovascular health, mounting evidence indicates a favorable effect on obesity and type 2 diabetes, as well. While health promotion strategies aimed at preventing adult obesity are emphasizing components of Mediterranean dietary patterns, a role for Mediterranean diets in attenuating the inflammatory burden associated with type 2 diabetes is also emerging. Moreover, a lower prevalence of the metabolic syndrome is associated with dietary patterns rich in fruits, vegetables, whole grains, dairy products, and unsaturated fats. Both epidemiological and interventional studies have revealed a protective effect of the Mediterranean diet against mild chronic inflammation and its metabolic complications. SUMMARY: Mounting evidence suggests that Mediterranean diets could serve as an anti-inflammatory dietary pattern, which could help fighting diseases that are related to chronic inflammation, including visceral obesity, type 2 diabetes and the metabolic syndrome.     

Alpha-blockers for the treatment of prostatitis-like syndromes

Prostatitis is a common medical diagnosis. The etiology of this symptomatic syndrome can be an acute or chronic bacterial infection, a noninfectious initiator (the most common cause), or iatrogenic heat or radiation; the syndrome may coexist with benign prostatic hyperplasia. Alpha-blockers have a role in the treatment of the prostatitis syndromes. In Category I, acute bacterial prostatitis, alpha-blockers have been shown to possibly ameliorate obstructive and irritative voiding symptoms. In Category II, chronic bacterial prostatitis, alpha-blockers seem to reduce the risk of clinical and bacteriological recurrence. In Category III, chronic pelvic pain syndrome, alpha-blockers improve symptoms and quality of life. Alpha-blockers also seem to ameliorate the symptoms and reduce the risk of acute urinary retention in patients who suffer from either heat- or radiation-induced prostatic inflammation. Alpha-blockers improve lower urinary tract symptoms, including pain, in patients who are diagnosed with both prostatitis and benign prostatic hyperplasia. Evidence has proven there is definitely a role for alpha-blockers in the management of the prostatitis syndromes.     

A global perspective on the crosstalk between saturated fatty acids and Toll-like receptor 4 in the etiology of inflammation and insulin resistance

Obesity is featured by chronic systemic low-grade inflammation that eventually contributes to the development of insulin resistance. Toll-like receptor 4 (TLR4) is an important mediator that triggers the innate immune response by activating inflammatory signaling cascades. Human, animal and cell culture studies identified saturated fatty acids (SFAs), the dominant non-esterified fatty acid (NEFA) in the circulation of obese subjects, as non-microbial agonists that trigger the inflammatory response via activating TLR4 signaling, which acts as an important causative link between fatty acid overload, chronic low-grade inflammation and the related metabolic aberrations. The interaction between SFAs and TLR4 may be modulated through the myeloid differentiation primary response gene 88-dependent and independent signaling pathway. Greater understanding of the crosstalk between dietary SFAs and TLR4 signaling in the pathogenesis of metabolic imbalance may facilitate the design of a more efficient pharmacological strategy to alleviate the risk of developing chronic diseases elicited in part by fatty acid overload. The current review discusses recent advances in the impact of crosstalk between SFAs and TLR4 on inflammation and insulin resistance in multiple cell types, tissues and organs in the context of metabolic dysregulation.