常见脂肪因子与银屑病相关病理机制

银屑病是一种与免疫相关的系统性炎症性皮肤病,近年来发现其与肥胖、高血压、糖尿病、代谢综合征、动脉粥样硬化等代谢性疾病相关。脂肪组织作为内分泌器官,可分泌多种脂肪因子参与炎症和代谢性疾病的发生发展,研究发现脂肪因子可能参与到银屑病的发病过程。本文通过回顾国内外文献,探讨常见脂肪因子与银屑病发病的关系,拟为银屑病提供新的诊疗和研究思路。     

脂肪因子与银屑病

银屑病发病机制涉及遗传、免疫等多种因素。近年来逐渐认识到银屑病是一种系统性疾病,与肥胖、高血压、糖尿病及代谢综合征等相关。脂肪组织可以通过分泌脂肪因子介导胰岛素抵抗、炎症调控、内皮功能障碍及动脉粥样硬化等异常。脂肪因子如瘦素、抵抗素、chemerin、脂联素及内脂素等在银屑病中表达异常,可能参与银屑病发病机制中的免疫应答及表皮异常增殖。     

部分炎症因子在银屑病与胰岛素抵抗相关性中的作用

近年来,研究学者认为银屑病易并发代谢性疾病,虽然二者发病机制尚未完全阐明,但是已发现银屑病和代谢性疾病的发病机理中有共同的炎症因子参与。一般认为,代谢性疾病是以胰岛素抵抗为共同病理生理改变的一系列炎症性疾病,本文主要就一些在银屑病发病机制与胰岛素抵抗中均起作用的炎症因子作简要综述。     

脂肪因子在银屑病中相关性的研究进展

脂肪组织可以通过分泌脂肪因子介导胰岛素抵抗、炎症调控、内皮功能障碍及动脉粥样硬化等异常。近年来逐渐认识到银屑病是一种系统性疾病,与肥胖、高血压、糖尿病及代谢综合征等相关。脂肪因子抵抗素、内脂素、网膜素及视黄醇结合蛋白4等在银屑病等皮肤病中表达异常,可能参与银屑病发病机制中的免疫应答及表皮异常增殖。     

脂肪因子和银屑病皮肤炎症及代谢异常相关性的研究进展

脂肪因子是由白色脂肪组织分泌的一系列生物活性物质,参与脂质和糖类代谢、炎症反应、凝血过程与血管稳态的调节。目前越来越多的研究发现,银屑病患者血浆及局部皮损中多种脂肪因子表达失衡,提示脂肪因子可能作为炎症递质和代谢功能调控因子,在银屑病的皮肤炎症与代谢异常中发挥重要作用。     

常见脂肪因子与银屑病相关的免疫学研究进展

银屑病是一种常见的慢性系统性炎症性疾病,病因不清。近年来发现脂肪因子可能广泛参与银屑病的发生与发展。本文对瘦素、脂联素、内脂素等常见脂肪因子及其受体的生物学特性和作用机制进行了介绍,并结合国内外文献,从免疫学的角度探讨了脂肪因子与银屑病发病之间的关系。     

银屑病与脂代谢相关性的研究进展

银屑病常伴发或伴发于多种代谢相关性疾病.脂肪组织是一种可分泌多种脂肪因子的内分泌器官,参与人体脂代谢、糖代谢、血管生成和炎症过程的调节.肥胖中促炎性因子和抗炎性因子的不平衡导致慢性炎症状态的发生、发展,可能是引起银屑病皮损恶化和治疗抵抗的原因之一.此外,皮脂腺细胞与脂肪细胞具有非常类似的作用,在细胞水平上将脂质代谢与炎症联系在一起.     

银屑病与糖尿病相关性研究北大核心CSCD

银屑病是慢性炎症性疾病,银屑病患者更易伴发糖尿病。有研究发现银屑病与糖尿病存在共同的致病基因,并且两者共享相似的基因突变。目前已知银屑病中所发生的炎症反应能促进胰岛素抵抗,而胰岛素抵抗是糖尿病、高血压、脂质代谢异常、心血管疾病等代谢性疾病的主要病理生理基础。另一方面,与糖尿病发病密切相关的脂肪因子可发挥免疫调节作用,进一步促进银屑病的发生。同时,不良生活方式也是两种疾病共有的危险因素。银屑病与糖尿病之间存在着生物学基础的关联,两者的相关性研究,有助于进一步了解银屑病的发病机制。     

肥胖及脂肪因子在银屑病发病中的作用

银屑病是一种免疫介导的慢性炎症性疾病,主要表现为反复出现的红斑鳞屑样皮损。银屑病的发病与遗传、环境和免疫等因素密切相关,其机制较为复杂,主要由促炎细胞因子驱动。与普通人群相比,银屑病患者的合并症风险增加,包括但不限于高血压、肥胖、糖尿病、代谢综合征（MS）、心血管疾病和抑郁症。脂肪组织作为一个大的内分泌器官,可通过产生多种促炎细胞因子和脂肪因子,从而引发各种下游效应。多项研究表明银屑病和肥胖症都代表着促炎状态并且这2种疾病的免疫机制有显著重叠,肥胖作为影响代谢的重要因素,已被证实可作为导致银屑病发病的一个独立危险因素。     

瘦素及其受体与银屑病相关性的研究进展

银屑病是一种T细胞介导的以角质形成细胞过度增殖为特征的慢性炎症性皮肤病,其发病机制尚未阐明,可能是由遗传因素、免疫因素、环境因素、肥胖等多种因素互相作用的多基因遗传病。近来,临床研究发现,银屑病伴发肥胖的比例增高,针对肥胖治疗后有助于银屑病好转,提示肥胖与银屑病密切相关。瘦素是参与机体代谢的脂肪因子,以往研究表明,瘦素与其受体在银屑病皮损中高表达,瘦素可能与银屑病的表皮过度增生相关,提示瘦素与银屑病和肥胖可能存在内在分子联系。     

Adipokines and psoriasis

Adipose tissue is an active endocrine organ contributing to the regulation of multiple metabolic pathways via self-produced bioactive products called adipokines. These adipokines are key players in the pathogenesis of metabolic syndrome and cardiovascular diseases. Co-occurrence of obesity and psoriasis could lead to interactions of both diseases in which adipokines, at least in part, are involved and may contribute to associated comorbidities of psoriasis. Until today numerous adipokines have been identified of which the most important ones are discussed in the following within the context of obesity, chronic inflammation and their possible role in the pathogenesis of psoriasis. Adipokines could serve as a missing link in the causal relationship between psoriasis and comorbidities and may provide a biomarker for disease severity, risk of comorbidities and treatment success.     

Leptin,adiponectin, visfatin and retinol‐binding protein‐4 – mediators of comorbidities in patients with psoriasis?

White adipose tissue is known to be involved in numerous physiological processes such as insulin-mediated functions, lipid and glucose metabolism, vascular changes and coagulation. These processes are mainly mediated by adipokines that are secreted either from adipocytes or cells of the stromal-vascular fraction of adipose tissue. In obesity, a shift in the production of adipokines can mediate the development of associated diseases, such as metabolic syndrome, and vascular complications, such as artherosclerosis, myocardial infarction or stroke, which are known comorbidities of psoriasis too. As obesity is a frequently seen comorbidity in psoriasis patients, adipokines could be involved in the pathogenesis of psoriasis and/or its comorbidities either dependently or independently from obesity. Therefore, this study investigates the levels of four major adipokines in psoriasis patients compared with a control group of healthy volunteers without chronic inflammatory diseases in relation to body composition. Leptin, adiponectin (high molecular weight (HMW) and total adiponectin), visfatin and retinol-binding protein 4 (RBP4) have been analysed in 79 psoriasis patients and in 80 healthy volunteers. It was shown that HMW adiponectin (OR 1.3755; P = 0.0094) and visfatin (OR 1.1267; P = 0.0472) are independently increased, and RBP4 (OR 0.9884; P < 0.0001) is independently decreased in psoriasis. In conclusion, increased levels of HMW adiponectin and decreased levels of RBP4 could be a mechanism in a chronic inflammatory state that helps to protect against vascular and metabolic disorders, whereas the increase of the pro-inflammatory adipokine visfatin could lead to atherosclerosis and vascular disorders found in psoriasis.     

Clear association between serum levels of adipokines and T‐helper 17‐related cytokines in patients with psoriasis

Background. Psoriasis represents one of the T‐helper (Th)17‐mediated autoimmune diseases, and has been shown to be associated with metabolic syndrome (MetS). It has been reported that some adipokines and Th17‐related cytokines are altered in patients with psoriasis. Aim. To examine the relationship between levels of adipokines and Th17‐related cytokines in the serum of patients with psoriasis compared with healthy controls. Methods. We enrolled 30 patients with psoriasis and 30 normal controls in the study, and used ELISA to measure serum adipokines and Th17‐related cytokines. The association between each adipokine and each cytokine was determined using Pearson correlation analysis. Multiple regression analysis using all adipokines and Th17‐related cytokines as covariates was also performed. Results. Pearson correlation analysis showed a strong positive association between chemerin and resistin levels and between adiponectin and high molecular weight adiponectin in normal controls. By contrast, in patients with psoriasis, resistin levels were significantly positively associated with tumour necrosis factor‐α, while there was a strong negative association between retinol binding protein‐4 and interleukin (IL)‐6 levels. Interestingly, a marked positive correlation between IL‐22 and adiponectin was also found in patients with psoriasis. Leptin levels correlated positively with IL‐6 in patients with psoriasis, but this did not reach significance. The correlations identified by the multiple regression analyses were almost identical to those from the Pearson analyses. Conclusions. These data suggest that distinct interaction between adipokines and Th17 cytokines is involved in the pathogenesis of psoriasis.     

Kinetics of circulating Th17 cytokines and adipokines in psoriasis patients

Psoriasis is associated with an increase of Th17 cytokines, such as IL-17, IL-22, IL-21, and TNF-α, which are produced by Th17 cells. Adipokines are peptide hormones or cytokines secreted from adipose tissues and involved in the pathogenesis of metabolic syndrome (MS). Psoriasis patients have a high prevalence of the MS. In this study, we investigated the statistics of circulating Th17-related cytokines and adipokines in psoriasis patients. Our study identified the significant elevation of serum IL-6, IL-21, IL-22, and resistin levels in psoriasis patients. Increased serum levels of IL-22 and adiponectin were positively correlated with Psoriasis Area and Severity Index (PASI). In contrast, serum high molecular weight adiponectin levels were decreased in psoriasis and negatively correlated with PASI.     

银屑病与非酒精性脂肪性肝病相关性研究进展

研究报道银屑病和非酒精性脂肪性肝病（NAFLD）的发病机制中有共同参与的炎症及细胞因子，银屑病可增加NAFLD的发病风险。胰岛素抵抗、TNF-α及脂肪因子已被证实在银屑病合并NAFLD的发病中具有重要作用。本文对银屑病与非酒精性脂肪性肝病相关性研究进展进行了综述。     

The role of lipids in vitiligo and schizophrenia

The pathogenesis of vitiligo and schizophrenia has not been adequately clarified. We explore the role of lipids in these diseases. Both conditions have been associated with stress in several observations and studies. Research data indicate complex interactions between oxidative stress and metabolic syndrome—with lipid abnormalities being a significant component of the latter—in these diseases. The impaired membrane lipid homeostasis mechanism is related to the increased phospholipid remodeling caused by excessive oxidative stress in schizophrenia. We indicate that sphingomyelin is possibly involved in the pathogenesis of these diseases. Statins have anti-inflammatory and immunomodulating effects and an effect against oxidative stress. Preliminary clinical studies show that these agents may be beneficial in both vitiligo and schizophrenia, but their therapeutic value should be studied further.     

The triad psoriasis–obesity–adipokine profile

Psoriasis is a chronic inflammatory skin disease, often associated with overweight/obesity. The adipose tissue is a complex organ that secretes several adipokines, involved in the regulation of some metabolic processes, such as lipid metabolism, glucose homeostasis, angiogenesis, blood pressure and inflammation. In obesity, the distribution and function of adipose tissue, and the adipokine profile are altered. The unbalanced production of pro‐ and anti‐inflammatory adipokines in obesity, contributes to the development of a chronic low‐grade inflammation state, which seems to favour worsening of psoriasis lesion and a poorer response to treatment. In this review, we will debate published data concerning the current knowledge about the triad psoriasis–obesity–adipokine profile.