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Metabolic syndrome low-density lipoprotein

Metabolic syndrome low-density lipoprotein

Metabolkc Diabetes, A. Article PubMed Google Scholar Body Composition Analysis Cholesterol Education Program NCEP Expert Metabolic syndrome low-density lipoprotein on Detection, Syndro,e, and Treatment of High Blood Cholesterol in Adults Adult Treatment Panel III. Bonora EKiechl SWilleit JOberhollenzer FEgger GBonadonna RCMuggeo M Metabolic syndrome: epidemiology and more extensive phenotypic description.

Metabolic syndrome low-density lipoprotein -

Several studies have indicated that two measures of BMI and WC are closely correlated [ 18 , 35 ]. Most individuals with an abnormal BMI also have an abnormal WC.

The incidence of MetS increases with the reduction of HDL over time. People with high-normal and normal HDL were less susceptible than people with higher HDL to developing MetS. In the low HDL group, elevated blood pressure was a secondary risk factor.

More effective risk mitigation strategies are needed for people with low HDL to prevent those developing MetS. Samson SL, Garber AJ. Metabolic syndrome. Endocrinol Metab Clin N Am. Article Google Scholar. Del Brutto OH, Zambrano M, Penaherrera E, Montalvan M, Pow-Chon-Long F, Tettamanti D. Sheikhbahaei S, Fotouhi A, Hafezi-Nejad N, Nakhjavani M, Esteghamati A.

Serum uric acid, the metabolic syndrome, and the risk of chronic kidney disease in patients with type 2 diabetes. Metab Syndr Relat Disord.

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Download references. Funding: The Program of Natural Science Fund of China Serial Number: ; the Major Project of Natural Science Fund of Beijing Serial Number: All funding sources were independent and had no influence on the study design; the collection, analyses, and interpretation of our data; the writing of this report; or the decision to submit the article for publication.

School of Public Health, Capital Medical University, No. Beijing Municipal Key Laboratory of Clinical Epidemiology, Beijing, , China. Physical Examination Department, Beijing Tongren Hospital Affiliated to Capital Medical University, No. You can also search for this author in PubMed Google Scholar.

Correspondence to Xiuhua Guo. XL, LT, and KC contributed to the statistical analysis and interpretation of the data, drafting of the article, and critical revision of the article; ZW, DC and XG contributed to the study conception and design, acquisition of data, field investigation and quality control; XL, JG, HZ, XY, YW, JW, CW and LL contributed to the drafting of the article, and critical revision of the article; XG had full access of all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

All authors gave their final approval for the manuscript. Open Access This article is licensed under a Creative Commons Attribution 4. Reprints and permissions. Liu, X. et al. Association of high-density lipoprotein with development of metabolic syndrome components: a five-year follow-up in adults.

BMC Public Health 15 , Download citation. Received : 25 October Accepted : 25 February Published : 22 April Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative.

Skip to main content. Search all BMC articles Search. Download PDF. Abstract Background High-density lipoprotein HDL is associated with the incidence of metabolic syndrome MetS. Methods During the period to , 4, adults in Tongren and Xiaotangshan Hospitals in Beijing were included with no MetS, self-reported type 2 diabetes, or cardiovascular disease at baseline.

Results The incidence of MetS at follow-up was 3. Conclusions The incidence of MetS increased in parallel with the decrease in HDL. Background Metabolic syndrome MetS is a complicated medical condition that includes five components: high plasma glucose, high triglycerides, low high-density lipoprotein cholesterol, high blood pressure, and abdominal obesity.

Measurements and laboratory tests The participants underwent routine physical examinations including measurements of weight, height, blood pressure BP , and analyses of blood biochemistry parameters. Diagnosis of metabolic syndrome Diagnostic criteria for the assessment of MetS components were determined according to the Joint Interim Statement Criteria [ 17 ].

Association rule mining ARM ARM, also known as market basket analysis MBA , is a popular data mining method designed to identify groups of variables with respect to a specific target variable [ 15 ]. Layered approach for high-density lipoprotein levels at baseline HDL at baseline was categorised into two sub-groups according to the Joint Scientific Statement of MetS [ 17 ].

Statistical analysis Categorical data are presented as percentages, and continuous data as mean plus standard deviation SD. Ethics statement This study was approved by the Ethics Committee of the Capital Medical University of China, Beijing, and performed in accordance with the principles of the Declaration of Helsinki Reference No.

Consent Written informed consent was obtained from each patient for publication of this report and any accompanying images. Results At baseline, of the 4, subjects, Figure 1. Full size image. Figure 2. Figure 3. Discussion This cohort study, comprising 4, subjects in Beijing Tongren and Beijing Xiaotangshan Hospitals, focused on investigating how the incidence of MetS changed relative to HDL level and which MetS components tend to emerge and change during the 5-year follow-up period.

Conclusions The incidence of MetS increases with the reduction of HDL over time. Abbreviations HDL: High-density lipoprotein MetS: Metabolic syndrome CVD: Cardiovascular disease DM: Diabetes mellitus ARM: Association rule mining BP: Blood pressure SBP: Systolic blood pressure DBP: Diastolic blood pressure BMI: Body mass index WC: Waist circumference MBA: Market basket analysis SD: Standard deviation MCMC: Markov chain Monte Carlo.

References Samson SL, Garber AJ. Article Google Scholar Del Brutto OH, Zambrano M, Penaherrera E, Montalvan M, Pow-Chon-Long F, Tettamanti D. Article Google Scholar Sheikhbahaei S, Fotouhi A, Hafezi-Nejad N, Nakhjavani M, Esteghamati A.

Article CAS PubMed Google Scholar Gami AS, Witt BJ, Howard DE, Erwin PJ, Gami LA, Somers VK, et al. Article CAS PubMed Google Scholar Wang F, Ye P, Hu D, Min Y, Zhao S, Wang Y, et al. Article CAS PubMed Google Scholar Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults.

Article Google Scholar Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al. Article PubMed Google Scholar National Cholesterol Education Program NCEP Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults Adult Treatment Panel III.

In addition, the risk of CVD associated with the atherogenic metabolic triad remained significant even after adjustment for traditional risk factors such as LDL-cholesterol, triglyceride and HDL-cholesterol levels. Risk assessment includes a list of biological parameters wherein lipids play an important role, especially triglycerides and HDL-particles.

The traditional factors associated with the syndrome are obesity, insulin resistance, hyperglycemia, dyslipemia, hypertension and microalbuminuria. There is currently no consensus definition of the metabolic syndrome, although the clustering of metabolic abnormalities, such as central obesity, impaired glucose tolerance and type 2 diabetes, dyslipidemia and hypertension has been noted in certain patients for many years.

Recently more components of the syndrome have been proposed, including vascular inflammation, hypercoagulability, hyperuricemia and microalbuminuria. According to Reaven 1 it is necessary to make a distinction between metabolic syndrome as a diagnostic category and metabolic syndrome as a pathophysiologic entity designating a cluster of related metabolic abnormalities.

Studies over the last 25 years have provided the evidence that insulin resistance at the level of muscle and adipose tissue was the common abnormality that increased the likelihood of an individual developing, not only type 2 diabetes, but also cardiovascular disease 2.

The concept of the metabolic syndrome viewed as precursor to the development of both type 2 diabetes and cardiovascular disease has progressively emerged with a formal recognition by the World Health Organization WHO in and the National Cholesterol Education Program Adult Treatment Panel III in NCEP ATP III , which has recently proposed a formal definition of the metabolic syndrome.

Over years several reports have been published indicating that the common ingredient has been insulin resistance, and it has been speculated that it may be mediated in part by an increase in FFA accompanied by an overproduction of triglyceride-enriched particles and increased small dense LDL particles.

In the prospective Cardiovascular Munster study PRO-CAM , male participants were examined for cardiovascular risk factors and kept under observation to record mortality and cardiovascular events including myocardial infarction and stroke. The importance of the triad of high triglycerides, low HDL and elevated LDL cholesterol has been further supported by recent analysis of the Helsinki Heart Study 7.

For practical purposes, it appears advisable to base risk prediction of atherosclerotic coronary artery disease and treatment decision on a full lipid profile rather than cholesterol alone or LDL-cholesterol determination.

In order to understand the role of hyperlipemia in the development of CHD, it is important to examine what happens at the endothelial level. LDL-cholesterol passes across the endothelium and is modified by stimulating macrophage chemoattractant protein-1 MCP-1 to recruit monocytes, and also by stimulating differentiation in macrophages which express scavenger receptors that take up lipid to make foam cells.

The foam cells produce growth factors and proteinases and they also release cytokines to stimulate adhesion proteins. HDL has multiple effects and can block the atherogenic process at several levels. The best known is the efflux of cholesterol from foam cells and the prevention of foam cell formation.

HDL also prevents the oxidizing modification of LDL within the intima. HDL has been shown to inhibit the cytokine-induced expression of adhesion proteins and to inhibit MCP It is also anti-thrombotic and anti-apoptotic.

Nofer has demonstrated that HDL exerts many anti-inflammatory effects, as illustrated in experimental models of atherosclerosis and in true models of inflammation. ApoA-I and lysosphingolipids can account for many of the anti-inflammatory effects of HDL. Oxidized low-density lipoprotein cholesterol ox-LDL may increase cytokine expression IL-1ß, TNF-α; IL-6 and IL-8 in endothelial cells.

This event is followed by vascular cell adhesion molecules, VCAM-1 and ICAM Isolated HDL and reconstituted HDL inhibit the expression of these cytokines in isolated endothelium cells. Further studies are underway to clarify the influence of HDL on the expression of endothelial cell adhesion molecules.

Among several causes of insulin resistance, it has been speculated that it may be mediated in part by an increase in free fatty acids FFA that inhibits post-insulin receptor signalling and thus contributes to insulin resistance. FFA may also be an important determinant of the metabolic syndrome as their level is generally high in this condition Figure 1.

As resistance to insulin action or insulin deprivation is associated with increased lipolysis, intra-abdominal fat, which is metabolically very active, releases FFA into portal circulation. The liver converts FFA into triglycerides and this may explain the relationship of hypertriglyceridemia and the metabolic syndrome.

Increased supply of glucose and overproduction of VLDL raises the concentration of triglyceride-enriched particles, leading to a reciprocal exchange of fatty acids: cholesterol-esters are transferred to VLDL and chylomicron remnants, while triglycerides are transferred to LDL and HDL particles to form small-dense LDL and HDL.

These dense particles are well known for their high atherogenic potential. Figure 1. Mechanisms relating to insulin resistance and dyslipidemia. Besides available pharmacological remedies used to decrease insulin resistance, exercise and weight loss represent the key steps as they are widely implemental and rather inexpensive.

Exercising increases GLUT-4 receptors in skeletal muscles using glucose with a reduction in insulin resistance. Several growth factors and cytokines can modulate insulin post-receptor signaling.

While IGF-1 enhance insulin action mediated by its cellular receptor, FFA, TNF-α a pro-inflammatory cytokine mainly produced by activated macrophages , and leptin seem to have the opposite effect 8.

TNF-α impairs insulin signaling by serine phosphorylation of IRS-1 and inhibits insulin receptor tyrosine kinase activity, which leads to impaired downstream signaling 5.

As TNF-α plasma concentration is increased in obesity, sepsis and cancer, this may in part explain why patients presenting with these conditions often exhibit abnormal glucose metabolism. The action of leptin on glucose disposal seems to be more equivocal in increasing phosphorylation of IRS-1 and IRS-2; on the other hand, leptin seems to be associated with insulin resistance as a strong correlation has been found between plasma leptin levels and insulin resistance in obese people, inhibiting post-receptor insulin signaling and action.

One of the major risk factors in metabolic syndrome is dyslipidemia which can be related to a changed lipoprotein spectrum and to modified lipoproteins.

A first step in separation and identification of serum lipoprotein classes was ultracentrifugation. Goffman and Lindgren were the first to separate serum lipoproteins in different density classes based on density gradients Figure 2. Figure 2. They were able to characterize particle sizes and relate them to the risk in coronary heart events.

We have had to wait till now to understand more about the relationship between physical parameters of molecules and the risk for disease. It is a challenge for the future to explore the influence of physical parameters of a particle on the development of a disease, to find methods for diagnostic possibilities and also to explore the ways of treatment.

Ultracentrifugation performed by Gofman and Lindgren in the s i. in and introduced by Svedberg became the reference method for lipoprotein separation and is still the golden standard for lipoprotein separation, identification and classification.

Since the introduction of this method, we have known that LDL lipoproteins are present in most cardiovascular events and that HDLs are considered protective against CVD. Total cholesterol does not accurately predict the risk of CVD, the decision on treatment is based on LDL-cholesterol, but LDL heterogeneity may also be taken into account.

Small dense LDL particles are more atherogenic than large, buoyant LDL particles, and ox-LDL also increases atherogenicity. Particle dimensions are very soon to become a diagnostic tool. Gradient gel electrophoresis without the use of denaturing conditions is commonly applied to characterize particle size distribution.

High-performance gel-filtration chromatography and nuclear magnetic resonance NMR spectroscopy have been recently applied for determinations of LDL particle size. Different methods of density gradient ultracentrifugation have been used to characterize LDL flotation rates, and several methods have been employed on discontinuous salt gradients to determine LDL subclasses based on density.

Various methods of determining LDL subclasses show a high degree of correlation despite the fact that they measure different physical properties of LDL. The new procedure exploits what appears to be natural but has generally been unappreciated, i.

proton NMR spectroscopic differences exhibited by lipoprotein particles of different sizes. The new process has now largely been complete. Using a dedicated intermediate-field MHZ NMR analyzer, routine quantification of 15 different subclasses of VLDL, LDL and HDL has been achieved in about one minute.

In the European Prospective Investigation into Cancer and Nutrition EPIC Study 9 , the relationship between LDL particle number and sizes were studied by NMR, together with LDL-cholesterol concentration and the risk of future coronary artery disease. LDL particle number was related to CAD also after adjustment for LDL-cholesterol concentration.

In figure 3, NMR profiles of lipoprotein distribution of two middle-aged patients A and B illustrate how different the underlying metabolic status and associated risk of CHD can be for two people who have virtually identical LDL and HDL cholesterol levels with, however, differences in CVD risk Figure 3.

Figure 3. NMR profiles of lipoprotein distribution of patients A and B. Nuclear magnetic resonance spectroscopy measures the plasma concentration of lipids in most lipoproteins, and it can be used to estimate particle concentration. The technique also measures the size of the lipoprotein particle.

Nevertheless, there is a direct relation between the size of the LDL particle and the rate of ox-LDL Small LDL particles are more susceptible to oxidation and ox-LDL is an independent risk factor for CVD.

The relationship between ox-LDL and different components of metabolic syndrome has been examined in a population study of 3. Also, the severity of individual components was evaluated Ox-LDL was measured against ODS ratio of cardiovascular disease.

The ox-LDL levels increased not only in function of the number of metabolic syndrome components but also in function of the severity of individual components Figure 4. Monoclonal antibody mAB-4E6 formed against a neo-epitope in the aldehyde substituted by apo-B in mice is used in the ELISA competition for determination of circulating ox-LDL.

As a conclusion, ox-LDL can be used as a marker for the analysis of cardiovascular risk in metabolic syndrome Figure 4.

Ox-LDL in function of the metabolic syndrome components. high LDL-cholesterol, hypertension and diabetes mellitus etc. Recent evidence has shown that the presence of metabolic syndrome is associated with an increased risk of coronary heart disease CHD , myocardial infarction, and stroke in both sexes.

This substantially increased risk of CV morbidity and mortality associated with the presence of metabolic syndrome appears independent of other significant, potentially confounding factors such as smoking, plasma LDL cholesterol levels or alcohol consumption.

Individuals with metabolic syndrome, particularly those with abdominal obesity, exhibit a highly atherogenic lipid profile which may account for their high risk of CVD. Central fat accumulation and the presence of insulin resistance have both been associated with a cluster of dyslipidemic features, i.

These abnormalities of lipoprotein metabolism are more likely to occur together than separately and constitute the key component traits of the metabolic syndrome. Recent prospective studies indicate that elevated triglycerides are an independent risk factor in CHD. Hypertriglyceridemia is associated with several atherogenic factors including increased concentrations of triglyceride-enriched lipoproteins and the atherogenic lipoprotein phenotype consisting of small dense LDL particles and low high-density lipoprotein HDL cholesterol.

The factors contributing to hypertriglyceridemia in general population include obesity, overweight, physical inactivity, excess alcohol intake, high-carbohydrate diet, type 2 diabetes, and some other diseases e. chronic renal failure, nephrotic syndrome , certain drugs e.

corticosteroids, estrogens, retinoids, high doses of adrenergic blocking agents , and genetic disorders familial combined hyperlipidemia, familial hypertriglyceridemia, and familial dysbetalipoproteinemia. In daily practice, elevated serum triglycerides are predominantly observed in persons with metabolic syndrome.

Many previous studies have indicated that hypertriglyceridaemia is strongly associated with all metabolic syndrome components.

Patients with metabolic syndrome who have hypertriglyceridemia most often exhibit elevated level of triglyceride-enriched lipoproteins which are considered atherogenic. In clinical practice, VLDL cholesterol is the most readily available measure of atherogenic remnant lipoproteins.

Thus, VLDL cholesterol can be a target of cholesterol-lowering therapy. Table 1. Abnormalities associated with hypertriglyceridemia in metabolic syndrome. Low levels of HDL-cholesterol are associated with increased risk of coronary artery disease CAD.

Sugar consumption and skin health liw-density about author. DOI: Categories: Review. PDF Article download : times. FB Share. Copyright © - Croatian Society of Medical Biochemistry and Laboratory Medicine. Official Low-deensity use. gov Lipoprotdin. gov website Performance support supplements to an official government organization in the United States. Lower cholesterol for heart health website. Share sensitive information only on official, secure websites. Metabolic syndrome is the name for a group of risk factors for heart diseasediabetesand other health problems. You can have just one risk factor, but people often have several of them together. Metabolic syndrome low-density lipoprotein

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