The metabolic syndrome: should current criteria influence clinical practice?

PURPOSE OF REVIEW: Many studies have recommended use of metabolic syndrome as an 'alternative' means to assess vascular disease risk, but few have been rigorous, leading to confusion amongst physicians regarding risk screening. This review critically appraises this evidence and also evaluates the data linking metabolic syndrome to type 2 diabetes. RECENT FINDINGS: Although presence of metabolic syndrome predicts vascular events, such prediction is inferior and does not enhance simpler Framingham-based risk scores which can be determined using nonfasting blood samples. The dichotomous nature of metabolic syndrome criteria and lack of age, low-density lipoprotein cholesterol, and smoking in part account for their inferior predictive ability. Metabolic syndrome criteria better predict type 2 diabetes but diabetes screening, if adopted, will likely require a two-stage process, with the first stage not dependent on blood sampling. Nevertheless, recent interest in metabolic syndrome has contributed to greater interaction between diabetologists and cardiologists and highlighted more strongly the relevance of obesity to vascular risk. SUMMARY: Best evidence suggests that current metabolic syndrome criteria should not be used as an alternative to established charts for risk prediction for vascular disease. Clinical focus should remain on established risk factors to determine and reduce risk of vascular events.     

Oxidative stress and metabolic syndrome

Metabolic syndrome is a collection of cardiometabolic risk factors that includes obesity, insulin resistance, hypertension and dyslipidemia. Although there has been significant debate regarding the criteria and concept of the syndrome, this clustering of risk factors is unequivocally linked to an increased risk of developing type 2 diabetes and cardiovascular disease. Metabolic syndrome is often characterized by oxidative stress, a condition in which an imbalance results between the production and inactivation of reactive oxygen species. Reactive oxygen species can best be described as double-edged swords; while they play an essential role in multiple physiological systems, under conditions of oxidative stress, they contribute to cellular dysfunction. Oxidative stress is thought to play a major role in the pathogenesis of a variety of human diseases, including atherosclerosis, diabetes, hypertension, aging, Alzheimer's disease, kidney disease and cancer. The purpose of this review is to discuss the role of oxidative stress in metabolic syndrome and its major clinical manifestations (namely coronary artery disease, hypertension and diabetes). It will also highlight the effects of lifestyle modification in ameliorating oxidative stress in metabolic syndrome. Discussion will be limited to human data.     

Metabolic syndrome and breast cancer: an overview

Worldwide, breast cancer is the most frequently diagnosed life-threatening cancer in women and the most important cause of cancer-related deaths among women. This disease is on the rise in Turkey. Metabolic syndrome is a cluster of metabolic disturbances including insulin resistance, dyslipidemia, hypertension, abdominal obesity and high blood sugar. Several studies have examined the association of the individual components of the metabolic syndrome with breast cancer. More recent studies have shown it to be an independent risk factor for breast cancer. It has also been associated with poorer prognosis, increased incidence, a more aggressive tumor phenotype. Basic research studies are now in progress to illuminate the molecular pathways and mechanisms that are behind this correlation. Given the fact that all of the components of metabolic syndrome are modifiable risk factors, preventive measures must be established to improve the outcome of breast cancer patients. In this review we set the background by taking into account previous studies which have identified the components of metabolic syndrome individually as breast cancer risk factors. Then we present the latest findings which elaborate possible explanations regarding how metabolic syndrome as a single entity may affect breast cancer risk.     

Adiponectin and visceral fat associate with cardiovascular risk factors

Objective: To examine the combined effect of CT‐measured visceral fat area (VFA) and adiponectin level against the clustering of metabolic risk factors. Design and Methods: The subjects were 6,996 Japanese. The subjects were divided according to the combinations of VFA and adiponectin level quartiles and the odds ratio for multiple risk factors of metabolic syndrome were calculated (adjusted for age and lifestyle factors using logistic regression analyses). Group with the lowest VFA and the highest adiponectin level was used as a reference. The correlation between adiponectin level and each metabolic risk factor was evaluated. Results: The strongest correlation was observed between adiponectin level and high‐density lipoprotein cholesterol levels (r = 0.369 and 0.439 for men and women). Both VFA and adiponectin level were independently associated with the clustering of metabolic risk factors (interaction P = 0.58 and 0.11 for men and women). The odds ratio for the clustering of metabolic risk factors in the group with the highest VFA and the lowest adiponectin level, compared with the group with the lowest VFA and the highest adiponectin level, was 12.7 (9.7‐16.6) for men and 13.5 (6.0‐30.2) for women. Conclusion: The ability to detect metabolic syndrome could be improved by examining adiponectin level in conjunction with VFA.     

中西医治疗代谢综合征的认识发展过程

代谢综合征是一系列代谢紊乱的状态和疾病。近年来代谢综合征在心脑血管疾病中的作用越来越引起学者们的重视。目前,腹型肥胖和胰岛素抵抗被认为是代谢综合征的核心因素,另外也有众多研究揭示了代谢综合征的其他致病机制。各个国家也在出台相应的诊断标准,这些标准都将指导临床的诊断及分型。在治疗方面,西药尚缺乏有效的综合治疗手段,已经有很多研究证实中药治疗疗效显著,复方治疗或单味药治疗均可以明显改善代谢综合征的症状。本文就中医及西医对于代谢综合征的各种认识的发展过程及其相应的治疗手段治疗做一综述。     

Diagnosis of the metabolic syndrome in children

PURPOSE OF REVIEW: The metabolic syndrome, a cluster of potent risk factors for atherosclerotic cardiovascular disease and type 2 diabetes mellitus in adults, is composed of insulin resistance, obesity, hypertension and hyperlipidemia. Of significant impact in the adult population, atherosclerotic cardiovascular disease and death are rarely seen in the young, but the pathologic processes and risk factors associated with its development have been shown to begin during childhood. The current review summarizes the work published during the past year in the following areas: childhood obesity, insulin resistance, dyslipidemia, hypertension and type 2 diabetes mellitus. RECENT FINDINGS: Recent studies have revealed the presence of components of the metabolic syndrome in children and adolescents. Obesity has a central role in the syndrome. There is an increasing amount of data to show that being overweight during childhood and adolescence is significantly associated with insulin resistance, abnormal lipids, and elevated blood pressure in young adulthood. Weight loss in these situations results in a decrease in insulin concentration and an increase in insulin sensitivity toward normalcy. With cardiovascular disease, obesity, and type 2 diabetes reaching epidemic proportions, it is of great importance to understand and control the risk factors at an early age. SUMMARY: The information obtained during the past year has improved our understanding of the pathogenesis, diagnosis and treatment of components of the metabolic syndrome in children, and potentially could improve the risk profiles for cardiovascular disease as children make the transition toward adolescence and young adulthood.     

Importance of diagnosing and treating the metabolic syndrome in reducing cardiovascular risk

Applying the criteria for the metabolic syndrome serves as a simple and inexpensive tool for identifying patients at high risk for diabetes and coronary heart disease, particularly those who do not fall into traditional risk categories. Several independent physiological processes underlie the non-random risk-factor clustering that defines the metabolic syndrome, including insulin resistance, central obesity, dyslipidemia, impaired glucose tolerance, and hypertension. Other non-classic risk factors, such as abnormal oxidized low-density lipoprotein-cholesterol, adiponectin, and C-reactive protein levels, are highly correlated with the metabolic syndrome. Use of the metabolic syndrome criteria for assessment is comparable with other risk-scoring systems in accurately predicting cardiovascular disease risk and is simpler to implement in the clinic. Further research is needed to define the etiology of the metabolic syndrome.     

A major health hazard: the metabolic syndrome

The clustering of several metabolic and cardiovascular disease risk factors has been termed the metabolic syndrome. The metabolic syndrome seems to result from a collision between susceptible "thrifty genes" and a society characterized by an increased prevalence of obesity and a sedentary lifestyle. The typical patient is characterized by abdominal obesity, a varying degree of glucose intolerance, dyslipidemia and often hypertension. The components of the metabolic syndrome are associated with insulin resistance, disturbances of coagulation and fibrinolysis, endothelial dysfunction and elevated markers of sub-clinical inflammation. The current review focuses mainly on the new definitions of the syndrome, the results of recent epidemiological studies and the consequences of the metabolic syndrome as an important risk factor for cardiovascular disease, premature death and diabetes. The metabolic syndrome constitutes a major challenge for public health professionals in the field of preventive medicine since more than 40 million U.S. adults seem to be affected by the syndrome. Lifestyle changes could have a profound influence on the syndrome and its development.     

Metabolic syndrome in children and adolescents--risk for sleep-disordered breathing and obstructive sleep-apnoea syndrome?

The clinical relevance of the term "metabolic syndrome", the definition criteria, and predictive power are being disputed. Inclusion of sleep-disordered breathing and sleep apnoea into a definition of metabolic syndrome is also controversial once children and/or adolescents are affected. Nevertheless, along with the increasing prevalence of childhood obesity, the prevalence of the metabolic syndrome in obese children is reported at 30%, irrespective of the definition applied. Moreover, childhood obesity is associated with sleep-disordered breathing. Adipocytokines, cytokines secreted from adipose tissue, are thought to play a major role in the pathophysiology of metabolic syndrome. Leptin was initially suggested as a promising "anti-obesity" hormone. New concepts indicate that in humans leptin and its soluble receptor may be more important in states of energy deficiency rather than a predictor of the metabolic syndrome. Adiponectin, on the other hand, is not only related to obesity and insulin resistance, but appears to be the strongest predictor for metabolic syndrome, even in children. In newborns and infants, both adipocytokines occur in high concentrations, even though this cannot completely explain the increased risk for ensuing metabolic disease later in life. Finally, low-grade systemic inflammation may underlie the clustering of metabolic risk factors. Overall factors from the adipose tissue may constitute not only markers but also mediators of metabolic sequelae of obesity.     

A comparison of different approaches to unravel the latent structure within metabolic syndrome

Background

Exploratory factor analysis is a commonly used statistical technique in metabolic syndrome research to uncover latent structure amongst metabolic variables. The application of factor analysis requires methodological decisions that reflect the hypothesis of the metabolic syndrome construct. These decisions often raise the complexity of the interpretation from the output. We propose two alternative techniques developed from cluster analysis which can achieve a clinically relevant structure, whilst maintaining intuitive advantages of clustering methodology.

Methods

Two advanced techniques of clustering in the VARCLUS and matroid methods are discussed and implemented on a metabolic syndrome data set to analyze the structure of ten metabolic risk factors. The subjects were selected from the normative aging study based in Boston, Massachusetts. The sample included a total of 847 men aged between 21 and 81 years who provided complete data on selected risk factors during the period 1987 to 1991.

Results

Four core components were identified by the clustering methods. These are labelled obesity, lipids, insulin resistance and blood pressure. The exploratory factor analysis with oblique rotation suggested an overlap of the loadings identified on the insulin resistance and obesity factors. The VARCLUS and matroid analyses separated these components and were able to demonstrate associations between individual risk factors.

Conclusions

An oblique rotation can be selected to reflect the clinical concept of a single underlying syndrome, however the results are often difficult to interpret. Factor loadings must be considered along with correlations between the factors. The correlated components produced by the VARCLUS and matroid analyses are not overlapped, which allows for a simpler application of the methodologies and interpretation of the results. These techniques encourage consistency in the interpretation whilst remaining faithful to the construct under study.     

Body size phenotypes and inflammation in the Women's Health Initiative Observational Study

Individuals with "metabolically benign" obesity (obesity unaccompanied by hypertension, dyslipidemia, and diabetes) are not at elevated 10-year risk of cardiovascular disease (CVD) compared to normal weight individuals. It remains unclear whether these obese individuals or normal weight individuals with clustering of cardiometabolic factors display heightened immune activity. Therefore, we characterized levels of acute-phase reactants (C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), white blood cell (WBC) count), adhesion molecules (E-selectin, vascular cell adhesion molecule-1), and coagulation products (fibrinogen, plasminogen activator inhibitor-1 (PAI-1)) among four body size phenotypes (normal weight with 0/1 vs. ≥2 metabolic syndrome components/diabetes and overweight/obesity with 0/1 vs. ≥2 metabolic syndrome components/diabetes) in cross-sectional analyses of 1,889 postmenopausal women from the Women's Health Initiative Observational Study (WHI-OS) nested case-control stroke study. Higher levels of all three inflammatory marker categories were found among women with overweight/obesity or ≥2 metabolic syndrome components or diabetes. Compared to normal weight women with 0 or 1 metabolic syndrome components, normal weight women with ≥2 metabolic syndrome components or diabetes were more likely to have ≥3 inflammatory markers in the top quartile (multivariate odds ratio (OR) 2.0, 95% confidence interval (CI): 1.3-3.0), as were overweight/obese women with 0 or 1 metabolic syndrome components (OR 2.3; 95% CI: 1.5-3.5). Overweight/obese women with ≥2 metabolic syndrome components or diabetes had the highest OR (OR 4.2; 95% CI: 2.9-5.9). Despite findings that metabolically benign obese individuals are not at increased 10-year risk of CVD compared to normal weight individuals, the current results suggest that overweight/obese women without clustering of cardiometabolic risk factors still possess abnormal levels of inflammatory markers.     

Metabolic and Body Composition Risk Factors Associated with Metabolic Syndrome in a Cohort of Women with a High Prevalence of Cardiometabolic Disease

BackgroundThe aetiology of the metabolic syndrome and the inter-relationship between risk factors for this syndrome are poorly understood. The purpose of this investigation was to determine the risk factors for metabolic syndrome and their interactions in a cohort of women with a high prevalence of metabolic syndrome.ResultsMetabolic syndrome was present in 49.6% of the study cohort. Logistic regression analysis demonstrated that adiponectin (odds ratio [95% CIs]: 0.84 [0.77, 0.92], p<0.0005) and abdominal subcutaneous fat (0.56 [0.39, 0.79], p = 0.001) reduced metabolic syndrome risk whilst insulin resistance (1.31 [1.16, 1.48], p<0.0005) and trunk fat-free soft-tissue mass (1.34 [1.10, 1.61], p = 0.002) increased risk. Within this group of risk factors, the relationship of adiponectin with metabolic syndrome risk, when analysed across adiponectin hexiles, was the least affected by adjustment for the other risk factors.ConclusionsAdiponectin has a significant protective role against metabolic syndrome and is independent of other risk factors. The protective and possible augmentive effects of abdominal subcutaneous fat and lean trunk mass, respectively on metabolic syndrome risk demonstrate the existence of novel interactions between body composition and cardiometabolic disease.     

LIPGENE: an EU project to tackle the metabolic syndrome

LIPGENE is a new 5-year sixth framework EU project involving researchers from 14 EU countries. It will contribute to a reduction in the economic and social burden of the metabolic syndrome through research that will optimise the health impacts of dietary fat change. LIPGENE aims to: account for variation in genotype response to fatty acid modification; enable greater availability of food products that can enhance human health; enhance consumer awareness, and motivate adoption of dietary approaches to disease prevention. A truly integrated programme, LIPGENE incorporates human nutrition, animal nutrition, plant biotechnology, and economic and social/consumer sciences. The human nutrition packages will utilise data from an existing prospective study (SUVIMAX) to identify genotype and dietary interactions as risk factors for the metabolic syndrome. A multi-centre intervention will examine the effects of dietary fat on various risk factors for the metabolic syndrome, while molecular investigations will be supported by mechanistic and functional studies. The British Nutrition Foundation, as dissemination partners for this EU programme, is initiating a wide-reaching programme to disseminate information about the project and its findings. Further details, including lists of upcoming project-related events, are available at www.lipgene.tcd.ie and www.nutrition.org.uk/lipgene.     

AMP-activated protein kinase: an emerging drug target to regulate imbalances in lipid and carbohydrate metabolism to treat cardio-metabolic diseases: Thematic Review Series: New Lipid and Lipoprotein Targets for the Treatment of Cardiometabolic Diseases

The adenosine monophosphate-activated protein kinase (AMPK) is a metabolic sensor of energy metabolism at the cellular as well as whole-body level. It is activated by low energy status that triggers a switch from ATP-consuming anabolic pathways to ATP-producing catabolic pathways. AMPK is involved in a wide range of biological activities that normalizes lipid, glucose, and energy imbalances. These pathways are dysregulated in patients with metabolic syndrome (MetS), which represents a clustering of major cardiovascular risk factors including diabetes, lipid abnormalities, and energy imbalances. Clearly, there is an unmet medical need to find a molecule to treat alarming number of patients with MetS. AMPK, with multifaceted activities in various tissues, has emerged as an attractive drug target to manage lipid and glucose abnormalities and maintain energy homeostasis. A number of AMPK activators have been tested in preclinical models, but many of them have yet to reach to the clinic. This review focuses on the structure-function and role of AMPK in lipid, carbohydrate, and energy metabolism. The mode of action of AMPK activators, mechanism of anti-inflammatory activities, and preclinical and clinical findings as well as future prospects of AMPK as a drug target in treating cardio-metabolic disease are discussed.     

Cardiac Health in Women With Metabolic Syndrome: Clinical Aspects and Pathophysiology

Although the classical cardiovascular risk factors (e.g., smoking and hypertension) are becoming more effectively managed, a continuous increase of the so‐called “cardiometabolic risk” is noted. Starting from this century, the nomenclature “metabolic syndrome” has become more popular to identify a cluster of disorders including obesity, dyslipidemia, hypertension, and insulin resistance. It is a primary risk factor for diabetes and cardiovascular disease in both genders. Interestingly, the metabolic diseases display a distinct gender disparity with an apparent “female advantage” in the premenopausal women compared with age‐matched men. However, women usually lose such “sex protection” following menopause or affliction of metabolic syndrome especially insulin resistance. A controversy exists in the medical literature concerning whether metabolic syndrome is a real syndrome or simply a cluster of risk factors. Several scenarios are speculated to contribute to the gender dimorphism in the cardiovascular sequelae in patients with metabolic syndrome including sex hormones, intrinsic organ function, and the risk factor profile (e.g., hypertension, dyslipidemia, obesity, sedentary lifestyle, and atherogenic diet). With the alarming rise of obesity prevalence, heart problems in metabolic syndrome continue to rise with a distinct gender dimorphism. Although female hearts seem to better tolerate the stress insults compared with the male counterparts, the female sex hormones such as estrogen can interact with certain risk factors to precipitate myopathic changes in the hearts. This synthetic review of recent literature suggests a role of gender disparity in myopathic factors and risk attributable to each metabolic component in the different prevalence of metabolic syndrome.     

Acipimox reduces circulating levels of insulin and associated neutrophilic inflammation in metabolic syndrome

Metabolic syndrome is a proatherosclerotic condition clustering cardiovascular risk factors, including glucose and lipid profile alterations. The pathophysiological mechanisms favoring atherosclerotic inflammation in the metabolic syndrome remain elusive. Here, we investigated the potential role of the antilipolytic drug acipimox on neutrophil- and monocyte-mediated inflammation in the metabolic syndrome. Acipimox (500 mg) was orally administered to metabolic syndrome patients (n = 11) or healthy controls (n = 8). Serum and plasma was collected before acipimox administration (time 0) as well as 2-5 h afterward to assess metabolic and hematologic parameters. In vitro, the effects of the incubation with metabolic syndrome serum were assessed on human neutrophil and monocyte migration toward the proatherosclerotic chemokine CCL3. Two to five hours after acipimox administration, a significant reduction in circulating levels of insulin and nonesterified fatty acid (NEFA) was shown in metabolic syndrome patients. At time 0 and 2 h after acipimox administration, metabolic syndrome serum increased neutrophil migration to CCL3 compared with healthy controls. No effect was shown in human monocytes. At these time points, serum-induced neutrophil migration positively correlated with serum levels of insulin and NEFA. Metabolic syndrome serum or recombinant insulin did not upregulate CCR5 expression on neutrophil surface membrane, but it increased intracellular JNK1/2 phosphorylation. Insulin immunodepletion blocked serum-induced neutrophil migration and associated JNK1/2 phosphorylation. Although mRNA expression of acipimox receptor (GPR109) was shown in human neutrophils, 5-500 μM acipimox did not affect insulin-induced neutrophil migration. In conclusion, results suggest that acipimox inhibited neutrophil proatherosclerotic functions in the metabolic syndrome through the reduction in circulating levels of insulin.     

Accessing autonomic function can early screen metabolic syndrome

Background

Clinical diagnosis of the metabolic syndrome is time-consuming and invasive. Convenient instruments that do not require laboratory or physical investigation would be useful in early screening individuals at high risk of metabolic syndrome. Examination of the autonomic function can be taken as a directly reference and screening indicator for predicting metabolic syndrome.

Methodology and Principal Findings

The EZSCAN test, as an efficient and noninvasive technology, can access autonomic function through measuring electrochemical skin conductance. In this study, we used EZSCAN value to evaluate autonomic function and to detect metabolic syndrome in 5,887 participants aged 40 years or older. The EZSCAN test diagnostic accuracy was analyzed by receiver operating characteristic curves. Among the 5,815 participants in the final analysis, 2,541 were diagnosed as metabolic syndrome and the overall prevalence was 43.7%. Prevalence of the metabolic syndrome increased with the elevated EZSCAN risk level (p for trend <0.0001). Moreover, EZSCAN value was associated with an increase in the number of metabolic syndrome components (p for trend <0.0001). Compared with the no risk group (EZSCAN value 0–24), participants at the high risk group (EZSCAN value: 50–100) had a 2.35 fold increased risk of prevalent metabolic syndrome after the multiple adjustments. The area under the curve of the EZSCAN test was 0.62 (95% confidence interval [CI], 0.61–0.64) for predicting metabolic syndrome. The optimal operating point for the EZSCAN value to detect a high risk of prevalent metabolic syndrome was 30 in this study, while the sensitivity and specificity were 71.2% and 46.7%, respectively.

Conclusions and Significance

In conclusion, although less sensitive and accurate when compared with the clinical definition of metabolic syndrome, we found that the EZSCAN test is a good and simple screening technique for early predicting metabolic syndrome.     

Correlations of insulin resistance and neoplasms

Insulin resistance is a worldwide risk factor for the two most dangerous human disease groups; namely, for cardiovascular lesions and malignancies. The insulin resistance syndrome have five basic criteria: hyperglycemia, visceral obesity, elevated serum triglyceride level, low HDL-cholesterol level (dyslipidemia) and hypertension. Each of these criteria alone are risk factors for cancer, and they mean together a multiple risk. Insulin resistance of the liver, skeletal muscles, and fatty tissue leads to a reactive hyperinsulinemia by the increased secretory activity of the beta-cells. Insulin has diverse metabolic effects, and at the same time is a growth factor. It enhances the production and mitogenic activity of other, insulin-like growth factors, and leads to pathological cell proliferation. In the uncompensated phase of insulin resistance hyperglycemia appears, which promotes tumor genesis by several pathways. The elevated serum glucose level is advantageous for the increased DNA synthesis of the tumor cells. It provokes deliberation of free radicals, which will cause derangement of both the DNA and the enzymes having a role in the repair mechanisms. Hyperglycemia leads to a nonenzymatic glycation of protein structures, and the glycated products enhance the deliberation of free radicals, cytokines and growth factors. Insulin resistance means an enhanced risk for breast, pancreas, liver, colon, bladder, prostate and oral cavity cancers. The moderately increased fasting glucose level is also a risk factor for breast, stomach and colon cancers, even without manifestation of type 2 diabetes. Insulin resistance promotes tumor progression as well. In cancer patients with hyperglycemia or type 2 diabetes, the rate of tumor recurrence, metastatic spread and fatal outcome is higher as compared with the tumor patients without metabolic disease. The correlation between insulin resistance and tumor promotion reveals new possibilities in the prevention and treatment of cancer. The healthy diet, physical activity and weight loss increase insulin sensitivity, and decrease the risk for both cardiovascular diseases and malignancies.     

Metabolomics: building on a century of biochemistry to guide human health

Medical diagnosis and treatment efficacy will improve significantly when a more personalized system for health assessment is implemented. This system will require diagnostics that provide sufficiently detailed information about the metabolic status of individuals such that assay results will be able to guide food, drug and lifestyle choices to maintain or improve distinct aspects of health without compromising others. Achieving this goal will use the new science of metabolomics – comprehensive metabolic profiling of individuals linked to the biological understanding of human integrative metabolism. Candidate technologies to accomplish this goal are largely available, yet they have not been brought into practice for this purpose. Metabolomic technologies must be sufficiently rapid, accurate and affordable to be routinely accessible to both healthy and acutely ill individuals. The use of metabolomic data to predict the health trajectories of individuals will require bioinformatic tools and quantitative reference databases. These databases containing metabolite profiles from the population must be built, stored and indexed according to metabolic and health status. Building and annotating these databases with the knowledge to predict how a specific metabolic pattern from an individual can be adjusted with diet, drugs and lifestyle to improve health represents a logical application of the biochemistry knowledge that the life sciences have produced over the past 100 years.     

脂肪组织功能失调在动脉血栓相关疾病中的作用

肥胖与代谢综合征是传统心血管疾病的危险因素.多项临床研究表明,肥胖也会增加患血栓性疾病(如急性心肌梗死和脑卒中)的风险.脂肪组织与血小板反应性增加和高凝状态形成以及纤溶功能降低等存在着重要联系.脂肪组织还是一个高度活跃的内分泌器官,其表达和分泌具有重要功能的脂肪因子和脂质代谢物参与调控全身代谢.深入地了解脂肪组织的内分...