脂联素与高血压相关性的研究进展

近年来的研究表明,脂肪组织是机体能量代谢过程中起关键作用的内分泌器官,它可分泌多种脂肪因子,其中脂联素是由脂肪细胞分泌的一种血浆激素蛋白,是迄今为止所发现的唯一与肥胖呈负相关的细胞因子,具有重要的生理功能,影响体内代谢和某些疾病的发生发展。脂联素可能通过多方面因素影响血压的变化,高血压患者体内血浆脂联素水平降低越来越受到重视,脂联素及其受体可能成为防治高血压病等心血管疾病的新靶点。     

脂联素与慢性肝病的关系研究进展

脂肪组织能够分泌多种脂肪因子,这些脂肪因子通过自分泌方式调节脂肪合成和分解代谢。脂联素是脂肪因子的一种,它除了能够促进糖和脂肪代谢之外还具有抗炎,增敏胰岛素和抗动脉粥样硬化等功能因而备受关注。一、脂联素与慢性肝病脂联素是在脂肪组织中特异表达的脂肪因子。在血浆中,脂联素以低分子量多聚体和高分子量多聚体的形式存在。脂联素存在两种受体:AdipoR1和AdipoR2。这两种受体在多种组织都有表达,但主要分布在骨骼肌和肝脏。血清脂联素水平与体脂肪含量、空腹胰岛素浓度、血浆甘油三酯水平密切相关。过氧化物酶激活物增值受体γ(P…     

内脂素在心血管疾病中的研究现状

脂肪组织是机体的能量储存场所,近年研究发现其还是一种大型的内分泌组织,可通过分泌内脂素、瘦素和脂联素等脂肪因子,参与调节机体的多种生物功能。内脂素（visfatin）是一种由白色脂肪组织分泌的新型脂肪因子,作为多功能蛋白质,其与心血管疾病的发生发展密切相关,如参与炎症反应、内皮功能障碍、血管重塑等病理生理过程。近年来,内脂素与心血管疾病逐渐成为热点,本文将从内脂素的生理特性及其与心血管疾病的关系进行综述,从而为防治心血管疾病提供新思路。     

脂联素与抵抗素对动脉粥样硬化的作用及其与血管紧张素受体拮抗剂关系

<正>大部分脂肪因子通过自分泌和旁分泌途径促进血管局部和远端炎性反应,然而同样有脂肪细胞的脂联素却具有相反作用〔1〕。脂联素血症是动脉粥样硬化(AS)发展的独立危险因子。抵抗素最初被认为是联系肥胖、胰岛素抵抗和2型糖尿病的新型脂肪因子,然而最近研究表明抵抗素可以作用于血管内皮细胞及平滑肌细胞从而影响其功能,促进AS的发生与发展〔2〕。而脂联素与抵抗素在对AS的作用中都部分性地通过核     

脂联素的抗动脉粥样硬化作用

动脉粥样硬化是一种以慢性轻度炎症为特征的疾病。脂联素是一种由脂肪细胞分泌的血浆蛋白,具有改善胰岛素敏感性、保护内皮功能、抗炎、抗动脉粥样硬化等作用。脂联素是目前唯一被证明与心血管疾病呈负相关的一种抗炎因子,本文就脂联素的抗动脉粥样硬化作用作一综述。     

脂联素与慢性肝病的研究进展

脂联素是主要由脂肪组织分泌的细胞因子,对机体存在广泛保护作用,也是唯一发挥保护作用的脂肪因子,可防止肝脏脂肪的积累。同时,脂联素具有抗炎、抗纤维化特性,可以对抗肿瘤坏死因子-α(TNF-α)及胰岛素抵抗,从而发挥对肝脏的保护作用,越来越多的学者开始研究将脂联素用于慢性肝病的治疗。此文着重就脂联素与常见慢性肝病,包括酒精性脂肪肝、非酒精性脂肪肝(NAFLD)、病毒性肝炎的研究进展作一综述。     

脂联素及其受体在酒精性肝病中的作用

脂联素是脂肪细胞特异分泌的一种脂肪因子,具有抗炎、促进脂肪酸氧化、减轻胰岛素抵抗等作用,在酒精性肝病患者及动物模型中,脂联素水平均下降,提示脂联素在酒精性肝病的发病中可能起重要作用,进一步研究其具体作用将为酒精性肝病的防治提供新的思路.     

脂联素在动脉粥样硬化中的抗炎性作用

脂联素是新近发现的一种由脂肪组织特异性分泌的脂肪因子,具有增加胰岛素敏感性、抗炎、抗动脉粥样硬化等作用,脂联素浓度与诸多炎症性疾病,特别是冠状动脉性心脏病(冠心病)进程密切相关。通过药物干预提高血浆脂联素浓度可能成为一种上述疾病的新的治疗方法。     

脂联素在心血管系统中的作用

脂联素是由脂肪细胞分泌的一种蛋白质,研究证实脂联素与胰岛素抵抗密切相关,具有抗动脉粥样硬化形成、抗炎症和损伤后抗内膜增生的特性。因此脂联素与糖尿病、心血管疾病密切相关,脂联素减少可作为冠心病的独立危险因子,补充脂联素可能是对上述疾病的一种新的治疗手段。     

C1q/肿瘤坏死因子相关蛋白9与心血管疾病关系的研究进展

正心血管疾病是目前导致人类死亡的主要病因之一,肥胖作为心血管疾病的重要危险因素,可导致脂肪组织分泌功能紊乱,加重罹患心血管疾病的风险[1]。脂肪因子主要由脂肪组织合成和分泌,包括脂联素(adiponectin,APN)、C1q/肿瘤坏死因子相关蛋白(C1q/TNF-related proteins,CTRPs)家族、瘦素(leptin)、抵抗素(resistin)等,可参与炎症反应、糖类及     

The metabolic syndrome is associated with circulating adipokines in older adults across a wide range of adiposity

BACKGROUND: Circulating levels of adipokines are elevated with adiposity and are closely linked with the clustering of traditional metabolic risk factors for cardiovascular disease. The purpose of this study was to examine the relationship of metabolic syndrome to several adipokines and the role of total and visceral adiposity in influencing this relationship in older adults. METHODS: A cross-sectional analysis was conducted including 1914 individuals aged 70-79 years without cardiovascular disease or type 2 diabetes. The metabolic syndrome was defined by the updated Adult Treatment Panel III criteria. Circulating levels of leptin, adiponectin, plasminogen activator inhibitor type 1 (PAI-1), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and C-reactive protein (CRP) were measured. Body composition and abdominal visceral fat area were determined. RESULTS: Both the presence of metabolic syndrome and the number of metabolic syndrome components were associated with higher levels of leptin, PAI-1, IL-6, TNF-alpha, and CRP and with lower levels of adiponectin (all p <.0001). The odds ratios for the prevalence of metabolic syndrome associated with adipokines were attenuated after adjustment for total fat mass and/or visceral fat area, but remained significant. Levels of leptin, PAI-1, IL-6, and TNF-alpha were higher (all p <.05 to p <.0001), and adiponectin was lower (all p <.0001), in persons with, compared to those without, metabolic syndrome within each tertile of percent body fat. CONCLUSION: The metabolic syndrome is associated with adipokines in older adults across a wide range of adiposity, including in those with low or normal overall fatness.     

Adipokine dysregulation,adipose tissue inflammation and metabolic syndrome

Obesity plays a causative role in the pathogenesis of the metabolic syndrome. Adipokines may link obesity to its co-morbidities. Most adipokines with pro-inflammatory properties are overproduced with increasing adiposity, while some adipokines with anti-inflammatory or insulin-sensitizing properties, like adiponectin are decreased. This dysregulation of adipokine production may promote obesity-linked metabolic disorders and cardiovascular disease. Besides considering adipokines, this review will also highlight the cellular key players and molecular mechanisms involved in adipose inflammation. Targeting the changes in the cellular composition of adipose tissue, the underlying molecular mechanisms, and the altered production of adipokines may have therapeutic potential in the management of the metabolic syndrome.     

Adiponectin and cardiovascular inflammatory responses

Obesity is recognized as a cause of many metabolic and cardiovascular disorders through its ability to promote chronic systemic inflammation. Recent studies have found that adipose tissues secrete numerous cytokines that are referred to as adipokines. Although most adipokines induce inflammation, adiponectin inhibits inflammatory reactions and protects against metabolic and cardiovascular diseases. This review focuses on the anti-inflammatory properties of adiponectin in various experimental systems, especially with respect to cardiovascular diseases.     

Inflammation,insulin resistance,and obesity

Obesity, in particular visceral obesity, has strong associations with cardiovascular disease and is related to many factors that are constituents of the metabolic syndrome. Increasing evidence suggests that features of the metabolic syndrome, including visceral obesity, are associated with a low-grade inflammatory state. Indeed, visceral fat is a source of several molecules, such as leptin, adiponectin, tumor necrosis factor-α, and interleukin 6, that are collectively called adipokines. All of them may induce a proinflammatory state and oxidative damage, leading to initiation and progression of atherosclerosis. Reducedenergy diets might represent an effective and healthful approach for long-term weight loss in patients with metabolic syndrome by reducing the underlying inflammatory condition.     

Adiponectin and its gene variants as risk factors for insulin resistance, the metabolic syndrome and cardiovascular disease

The increasing prevalence of obesity and metabolic syndrome/insulin resistance has attracted considerable interest due to their identification as risk factors for cardiovascular disease and, hence, targets for cardiovascular disease prevention. This review focuses on adiponectin, the most profusely secreted protein from adipose tissue, which itself is being increasingly recognised as an important and very active endocrine organ, secreting a wide range of biologically active substances known as adipokines or adipocytokines. Adiponectin has been demonstrated to have insulin sensitising effects, and secretion of adiponectin is reduced as adipose tissue mass increases. Adiponectin has also been demonstrated to have anti-inflammatory and anti-atherogenic properties, and is independently associated with cardiovascular disease. The evidence that suggests adiponectin plays a role in the relationship between obesity and insulin resistance, and also insulin resistance and cardiovascular disease, is examined. Variation in the adiponectin gene is one tool to determine whether this relationship is causal. The association of identified variants with human disease, specifically obesity and its consequences, type 2 diabetes and cardiovascular disease is reviewed. This data may enable patients at greater risk of the adverse effects of obesity to be identified and, as such, benefit from more targeted therapy of its consequences.     

The link between abdominal obesity, metabolic syndrome and cardiovascular disease

AimThe prevalence of metabolic syndrome has increased dramatically in recent years, and the cluster of metabolic abnormalities it encompasses results in increased cardiovascular morbidity and mortality. The role of abdominal (visceral) obesity and the underlying molecular and cellular mechanisms central to this association have been the subject of intensive research in recent times. The aim of this review is to correlate data in this area, highlighting the central role of excess visceral fat and its secreted adipokines, and to review existing and emerging therapies.Data synthesisData were generated from a search of the PubMed database using the terms ‘abdominal obesity’, ‘metabolic syndrome’, ‘insulin resistance’, ‘adipokines’, ‘interleukin-6 (IL-6)’, ‘adiponectin’, ‘tumour necrosis factor-alpha (TNF-α)’ and ‘cardiovascular disease’.ConclusionMetabolic syndrome is associated with a pro-inflammatory state, and the role of visceral obesity is thought to be central to this. Visceral obesity leads to alteration of the normal physiological balance of adipokines, insulin resistance, endothelial dysfunction and a pro-atherogenic state. In association with this, the presence of conventional cardiovascular risk factors such as hypertension, dyslipidaemia and smoking results in a significantly elevated cardiovascular and metabolic (cardiometabolic) risk. Better understanding of the molecular mechanisms central to this association has led to the development of potential therapeutic agents.     

Association of the leptin to high-molecular-weight adiponectin ratio with metabolic syndrome

Recent studies have reported that leptin and adiponectin are associated with metabolic syndrome. The leptin/adiponectin ratio has been suggested as an atherosclerotic index. The objective of this study was to compare the degree of association of metabolic syndrome with adiponectin levels, leptin levels, leptin/adiponectin ratio, and leptin/high-molecular-weight (HMW) adiponectin ratio. The study population included 3272 Koreans (men: 1915, women: 1357; age, 30-84 years), who had visited the Health Examination Center. Adipokines were divided into quartiles, and metabolic syndrome was defined by the National Cholesterol Education Program Adult Treatment Panel-III (NCEP ATP III). A logistic regression model was fitted to establish the association between adipokines and metabolic syndrome. Adipokines, such as adiponectin, HMW adiponectin, and leptin, were found to be statistically related to metabolic syndrome. Compared to the lowest quartile, the leptin/HMW adiponectin ratio in the highest quartile was associated with a 5-fold increase in the probability of prevalent metabolic syndrome, which was independent of age, smoking status, exercise, low-density lipoprotein (LDL) cholesterol, and body mass index. There was a linear increase in the leptin/HMW adiponectin ratio as the number of metabolic syndrome components increased. The leptin/HMW adiponectin ratio had the highest odds ratio in women. In addition, compared to adiponectin or leptin alone, the AUC of the leptin/adiponectin ratio and leptin/HMW adiponectin ratio was higher for metabolic syndrome. We may suggest that the leptin/HMW adiponectin ratio is not superior to other adipokine markers, but is as effective as the leptin/total adiponectin ratio.     

Adipokines and cardiovascular risk in Cushing's syndrome

Cushing's syndrome (CS) is associated with increased cardiovascular morbidity and mortality. Recent evidence also suggests that increased cardiovascular risk may persist even after long-term remission of CS. Increased central obesity, a typical feature of CS, is associated with altered production of adipokines, which contributes to the pathogenesis of several metabolic and cardiovascular complications observed in this condition. In vitro and in vivo studies have shown a relationship between cortisol and adipokines in several experimental settings. In patients with either active or 'cured' CS, an increase in leptin and resistin levels as well as the release of pro-inflammatory cytokines, such as tumor necrosis factor-α and interleukin-6, may be associated with increased cardiovascular risk. For other adipokines, including adiponectin, results are inconclusive. Studies are needed to further elucidate the interactions between clinical and subclinical increases in cortisol production and altered adipokine release in CS.     

Associations of adiponectin, resistin, and tumor necrosis factor-alpha with insulin resistance

CONTEXT: Adipose tissue-derived adipokines may contribute to insulin resistance. OBJECTIVE: We tested the hypothesis that adipokines are associated with insulin resistance in a community-based cohort and that associations are maintained in people with and without the metabolic syndrome (high vs. low risk of diabetes). DESIGN, SETTING, AND PARTICIPANTS: We studied a cross-sectional sample of 2356 individuals attending the seventh examination (1998-2001) of the Framingham Offspring Study. We measured levels of glucose, insulin, adiponectin, resistin, and TNFalpha in fasting blood samples and defined metabolic syndrome by updated National Cholesterol Education Program criteria. We used ANOVA to test associations of adipokines with insulin resistance and multivariable logistic regression models to assess joint associations of adipokines and metabolic syndrome with insulin resistance. MAIN OUTCOME MEASURE: Homeostasis model (HOMA-IR), with insulin resistance defined by HOMA-IR greater than the 75th percentile, was measured. RESULTS: Age- and sex-adjusted HOMA-IR levels were inversely related to adiponectin (r = -0.40, P < 0.0001) and positively related to resistin (r = 0.13, P < 0.0001) and TNFalpha (r = 0.12, P < 0.0001). The prevalence of insulin resistance increased with decreasing tertiles of adiponectin (from 10.9% in the third to 42.5% in the first tertile; P < 0.0001) and increasing tertiles of resistin (from 19.3 to 30.9%; P < 0.0001) and TNFalpha (from 18.8 to 32.0%; P < 0.0001). Results were similar after adjustment for body mass index. These associations were present in individuals with or without the metabolic syndrome. In multivariable regression models, metabolic syndrome and adipokines individually and jointly were significantly associated with insulin resistance. CONCLUSION: Adverse levels of adipokines are associated with insulin resistance in individuals at low or high diabetes risk.     

Emerging role of adipokines as mediators in atherosclerosis

Atherosclerotic cardiovascular disease is a major health problem around the world. Obesity is a primary risk factor for atherosclerosis and is associated with increased morbidity and mortality of cardiovascular diseases. However, the precise molecular pathways underlying this close association remain poorly understood. Adipokines are cytokines, chemokines and hormones secreted by adipose tissue that couple the regulation of lipid accumulation, inflammation, and atherogenesis, and therefore serve to link obesity with cardiovascular disorders. Obesity-related disorders including metabolic syndrome, diabetes, atherosclerosis, hypertension, and coronary artery disease are associated with dysregulated adipokine(s) expression. Recent studies demonstrate the proinflammatory effects as well as atherogenic properties of adipokines. Adipokines also participate in the regulation of endothelial function, which is an early event in atherosclerosis. By contrast, adiponectin, an adipocyte-derived hormone, exerts anti-inflammatory, anti-atherogenic and vascular protective effects. Furthermore, there is an interactive association among adipokines, by which adipokines reciprocally regulate each other's expression. Understanding this interplay may reveal plausible mechanisms for treating atherosclerosis and coronary heart disease by modulating adipokine(s) expression. In this review, we discuss insights into the role and the therapeutic potential of adipokines as mediators of atherosclerosis.