Peer Review reports. 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.

MetS is associated with an increased risk of the development of cardiovascular disorders worldwide. Patients with MetS have a two-fold greater relative risk for cardiovascular disease CVD , a five-fold greater risk for type 2 diabetes mellitus DM , a 2.

A meta-analysis of , individuals demonstrated a significantly higher risk of cardiovascular events associated with MetS [ 4 ]. Lipid abnormalities, including low high-density lipoprotein HDL , in MetS may contribute substantially to these high cardiovascular risks [ 5 ].

It is not yet clear whether or not MetS has a single cause, although it is known that insulin resistance is a major underlying cause of MetS [ 6 - 8 ].

HDL has been shown to be a key component in the prediction of CVD risk and may trigger the pathogenesis of MetS [ 9 ]. A cross-sectional study indicated that the HDL sub-class ratio is strongly associated with HDL, insulin resistance, as well as other MetS components in Japanese individuals [ 10 ].

However, there have been few cohort studies investigating which MetS components tend to cluster dominantly, and how the status of each component changes over time [ 11 - 13 ]. These factors may hamper the adequacy of management among individuals with MetS.

Our previous study revealed that people with optimal and normal blood pressure were less susceptible to developing MetS over a five year period, whereas abnormal blood pressure seemed to be a pre-existing phase of MetS [ 14 ]. Multiple statistical methods, such as logistical regression, Cox proportional hazards regression model, a net-work approach, latent transition, and factor analysis were applied in the previous research [ 8 , 9 , 11 - 13 ].

However, these methods can not deal with independent variables that are correlated with each other. Thus association rule mining ARM , which is a popular data mining method designed to identify groups of variables that are strongly correlated with each other, or with respect to a specific target variable, was used in the present study [ 15 ].

The purposes of this study were to investigate: 1 whether or not there is a correlation between the level of HDL and the incidence of MetS; 2 which components tend to develop at each level of HDL; and 3 how these components change with time. In total, 6, people who had check-up records at both baseline and the follow-up were enrolled.

Firstly, people with any medical history of stroke, cerebral infarction, myocardial infarction, or coronary heart disease, or in use of any hypoglycaemic, anti-dislipidemic, or anti-hypertensive treatments were excluded.

Secondly, 13 people aged less than 20 years and people aged over 65 years were excluded. Lastly, subjects who had MetS at baseline were ruled out.

The final cohort was composed of 4, subjects. The participants underwent routine physical examinations including measurements of weight, height, blood pressure BP , and analyses of blood biochemistry parameters. Height and body weight were measured in the upright position to the nearest of 0. Electronic sphygmomanometers were used by a trained nurse to measure the BP of each subject in the sitting position after a minute rest period.

During the 30 min preceding the measurements, the subjects were required to refrain from smoking or consuming caffeine [ 16 ]. The readings of systolic blood pressure SBP and diastolic blood pressure DBP were recorded, when the second measurement was in an extent of 5 mmHg. Three systolic and diastolic blood pressures were recorded, with an interval of at least 1 minute between readings, and the average of the last two measurements was used for data analysis [ 16 ].

Blood samples were collected from an antecubital vein in the morning after an overnight fasting period and placed in tubes containing EDTA. The samples were analysed immediately after pre-treatment or stored at °C in the ISO accredited medical laboratories of the hospital for further analysis.

Serum HDL concentration was measured photometrically Hitachi ; Roche, Mannheim, Germany , and TG and FPG concentrations were determined enzymatically Hitachi ; Roche Diagnostics. Diagnostic criteria for the assessment of MetS components were determined according to the Joint Interim Statement Criteria [ 17 ].

Body mass index BMI was regarded as a substitute for the component of obesity, which was strongly correlated with waist circumference WC in patients with MetS [ 18 ], as WC was not obtained.

The parameters used were as follows:. Participants fulfilling at least three out of these five components were diagnosed as having MetS. 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 ].

The strength of this method is that ARM measures the support and confidence, as explained below. The support rate of transitions is defined as the percentage of initial status to another status in all possible transitions, and the confidence rate represents the number of cases transitioned within a certain status.

In this study, support rate and confidence rate were used to evaluate which were the relatively frequent transition patterns and which status increased most, respectively. More details on the a priori algorithm underpinning ARM are available elsewhere [ 20 - 22 ].

HDL at baseline was categorised into two sub-groups according to the Joint Scientific Statement of MetS [ 17 ]. Categorical data are presented as percentages, and continuous data as mean plus standard deviation SD.

We performed ARM to analyse the changes in each MetS component or combinations thereof during the five-year period of this cohort study. As the subjects at baseline were people with two or fewer MetS components, there were 16 i. Theoretically there were i. A few values from biochemical sera were missing, thus a multiple imputation MI was performed to impute the missing information.

According to the data distribution, the Markov chain Monte Carlo MCMC method was chosen to avoid the loss of generality. All analyses were conducted using SAS software package Version 9. A 2-sided α of 0. Bonferroni adjustment of critical p-values was adopted when performing multiple comparisons.

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. Written informed consent was obtained from each patient for publication of this report and any accompanying images.

At baseline, of the 4, subjects, The follow-up interval was 4. The baseline characteristics are summarised in Table 1. The components of MetS in the population at baseline and follow-up were grouped by HDL level at baseline Tables 2 , 3 , 4 and 5.

Subjects were divided into two age groups 20 to 44 young and 45 to 65 old. The incidence of MetS at follow-up was analysed by gender and HDL level at baseline Figures 1 and 2.

Young men with high-normal and normal HDL levels had a higher incidence of MetS compared with women in the same groups 2. The numbers of young men and young women were almost the same in the low HDL group Whereas the numbers of old men and old women were almost the same in the high-normal, normal, and low HDL groups 4.

The accumulated incidence of MetS in subjects aged , stratified by gender and high-density lipoprotein level. The five most common transitions in each sub-group were identified Figure 3. As the sample size was too small after grouping by age, the association rule was applied without sub-stratification of age.

For visual simplicity, the five most commonly observed transitions are shown in the relevant parts of Figure 3. The rates of transition are shown for each gender and HDL group. The confidence rate represents how many cases transitioned within a certain status. For example, males were initially healthy at baseline, and A in high-normal HDL group of males; B in normal HDL group of males; C in low HDL group of males; D in high-normal HDL group of females; E in normal HDL group of females; F in low HDL group of females.

Abbreviations: H, health, with the absence of any MetS components; BP, high blood pressure; TG, raised triglycerides level; GLU, high fasting plasma glucose; HDL, increased high-density lipoprotein level. 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.

Our study identified that the lower the HDL at baseline, the higher the incidence of MetS at follow-up. We found that women with different levels of HDL would develop different combinations of MetS components.

On analysing the change in MetS components, we identified that those women with low HDL tended to have elevated blood pressure as the most common additional MetS component, while those women with higher HDL tended to have elevated HDL as the most common new-onset MetS component.

Men tended to have elevated blood pressure as the most common additional and new-onset MetS component. The HDL of people with normal-high and normal high-density lipoprotein at baseline tended to decrease with time, while the HDL increased in those subjects with low high-density lipoprotein, according to Tables 2 , 3 , 4 and 5.

Subjects with low high-density lipoprotein may be alert to their health as health education and promotion programmes are available through various media in Beijing, possible actions on exercise and diet could be intentionally or unintentionally taken, therefore their HDL is controlled or even higher.

An association between low HDL and MetS has been reported as the most prominent new onset MetS component, or even serves as a key component of predicting cardiovascular and diabetes risk [ 9 , 13 , 23 ]. Several studies with structural equation modelling showed that low HDL might play both a direct and indirect role in the progression of MetS [ 24 - 26 ].

However, physiologically, it is not easy to connect low HDL with MetS. In the present study, we found that people with high-normal and normal HDL tended to have a relatively lower incidence of MetS after five years when compared with people with low HDL, and were less susceptible to developing the disorder.

Most subjects who started off as healthy remained healthy, similar to a previous study amongst a German population [ 13 ]. However, lowered HDL tended to be the first risk factor of MetS for people with normal HDL, which is roughly confirmed in another population [ 13 ]. Low HDL-C level has been found to be independently and significantly related to myocardial infarction or stroke in patients with MetS, thus multi-factor treatment strategies, including strict life style change, should be made to improve dyslipidemia in MetS and decrease the residual risk for CVD in MetS [ 5 , 27 ].

The components of MetS tended to cluster in a way which varied from one population to another [ 13 , 28 ]. In our study, people with low HDL tended to have raised blood pressure as a secondary risk factor.

This is roughly consistent with other studies, which found that elevated blood pressure was the second most important component of MetS and people with MetS tended to have hypertension [ 14 , 23 ].

Low HDL seemed to be related to each of the other four components. It is mainly a consequence of systemic low-grade inflammation and apo A-I dysfunction. The aggregation to lipoprotein Lp a of apo A-I underlies HDL dysfunction, and is an independent risk factor of magnitude similar to conventional components of MetS [ 30 ].

Several studies showed that the steep increase in dyslipidemia could be the reason for the growing prevalence of diabetes and vice versa [ 23 , 31 ]. Dyslipidemia in patients with MetS may be caused by a combination of increased catabolism of HDL-apo A-I particles, overproduction of very LDL apo B, and decreased catabolism of apo B containing particles: these abnormalities may be consequences of insulin resistance [ 32 ].

An important link between obesity, the metabolic syndrome, and dyslipidemia, seems to be the development of insulin resistance in peripheral tissues leading to an enhanced hepatic flux of fatty acids from dietary sources, intravascular lipolysis, and from adipose tissue resistant to the antilipolytic effects of insulin [ 32 ].

Previous reports indicated that pro-inflammatory state and oxidative stress are crucial for evaluating cardiometabolic risk. Factors such as creatinine, platelet-activating factor acetyl hydrolase, thyroid stimulating hormone, acetylation-stimulating protein, asymmetric dimethylarginine, and serum lipoprotein Lp a are key to triggering systemic low-grade inflammation and enhanced autoimmune reactions, which may induce low HDL and metabolic syndrome [ 33 ].

Low HDL seemed to be a crucial status for MetS prevention. Since dyslipidemia has low rates of awareness, treatment, and control among Chinese adults, it is an important preventable risk factor for MetS and CVD events [ 34 ]. The strengths of this study were that it was a longitudinal study over five years in a Chinese population with data subject to relatively good quality control.

There were some limitations to this study. The first limitation of this study is the relatively small sample that might not be sufficiently representative of the general adult population and the demographics and referral source may limit the generalisation of the results.

Further studies using the general population would be desirable. Secondly, information about lifestyles was not available, but lifestyle variables will be included in further studies.

The third limitation is the lack of WC measurements as an indicator of central obesity. at their equivalent plasma concentrations, to take into account interindividual variation in plasma levels of HDL subfractions. Accumulation of conjugated dienes was measured as the increment in absorbance at nm 26 , The kinetics of diene accumulation revealed two characteristic phases, the lag and propagation phases.

For each curve, the duration of each phase, average oxidation rates within each phase and amount of dienes formed at the end of the propagation phase maximal amount of dienes were calculated.

Accumulation of TBARS was determined photometrically at nm after reaction with thiobarbituric acid The electrophoretic mobility of LDL was measured on 0. Non-Gaussian distributed variables were log transformed before statistical analysis.

All results are expressed as means ± sd. In contrast, no significant difference in sex ratio, DBP, and plasma level of apoA-I was found between the two groups.

In addition, the ratio of TC to HDL-C 6. BMI, Body mass index. Levels of systemic stress, assessed as plasma 8-isoprostanes, were 3. The quantitative distribution of HDL subfractions as percent mass tended to be distinct between MetS patients and controls, although no significant differences in absolute concentrations of HDL subfractions were found between the two groups Table 2.

When considering total HDL, a significantly lower percent content of CE Significantly lower concentrations of CE in HDL2b In contrast, concentrations of TG in HDL3a 4. By contrast, no difference between the two groups was found in the relative apoA-I, apoA-II, and apoC contents data not shown.

No difference in PON1 activity was found between corresponding HDL subfractions isolated from serum of MetS patients and controls. PAF-AH activity was also nonuniformly distributed between HDL subfractions in MetS patients and controls Table 2.

Furthermore, PAF-AH activity was significantly higher in MetS patients, compared with controls, in HDL2b, 2a, 3a, and 3b subfractions Table 2. When HDL subfractions isolated from controls Fig.

Such antioxidative activity of HDL subfractions was markedly impaired in MetS patients. Furthermore, the decrease in the production of conjugated dienes was significantly less pronounced in controls, in comparison with MetS patients Fig. LDL was incubated with AAPH 1 m m in the presence or absence of HDL subfractions in PBS at 37 C, and conjugated diene formation was measured by absorbance increment at nm.

incubation without added HDL. control subjects. More precisely, dense HDL3a, 3b, and 3c and light HDL2a subfractions from controls significantly decreased the oxidation rate in the propagation phase Fig. Note that large, light HDL subfractions tended to increase maximal diene production both in MetS patients and controls Figs.

Hence, the impairment in the oxidative protection of LDL by HDL subfractions in MetS patients was only observed after the lag phase, i. at late stages of LDL oxidation. In addition, the MetS HDL2a subfraction was significantly less potent in prolonging the propagation phase 83 vs.

The LDL oxidation rate in the presence of HDL3c positively correlated with insulin resistance assessed as the HOMA index Fig. Correlations between LDL oxidation rate in the propagation phase and insulin resistance assessed by the HOMA index A , between plasma 8-isoprostanes and antioxidative activity of HDL3c assessed by the rate of LDL oxidation in the propagation phase B , and between PON1 activity and antioxidative activity of HDL subfractions assessed by the rate of LDL oxidation in the propagation phase C.

By contrast, no significant correlation was found between the antioxidative activities of HDL subfractions and either apoA-I or apoA-II level data not shown. The present investigations have established that the antioxidative, antiinflammatory activity of small, dense HDL particles notably HDL3b and 3c is impaired in subjects exhibiting a MetS phenotype involving atherogenic dyslipidemia hypertriglyceridemia and subnormal HDL-C levels , hyperglycemia, hyperinsulinemia, hypertension, and central obesity.

Such deficient HDL antioxidative capacity was associated not only with markedly elevated systemic oxidative stress 3. Furthermore, correlational analysis revealed that the impaired antioxidative activity of small, dense HDL in MetS was intimately related to the presence of hypertriglyceridemia, hyperinsulinemia, and insulin resistance as HOMA index , thereby suggesting that abnormalities in both lipid and glucose metabolism underlie the antioxidative dysfunction of HDL particles in MetS.

Oxidative stress is defined as an imbalance between prooxidant and antioxidant factors in favor of prooxidants, thereby potentiating oxidative damage Furthermore, hypertriglyceridemia, hypertension, and obesity are each associated with increased production of superoxide anion via the nicotinamide adenosine diphosphate oxidase pathway 33 — In addition, hyperglycemia leads to elevated formation of oxygen free radicals as a consequence of protein glycation and glucose autoxidation 36 , Our correlational data strongly suggest then that small, dense HDL particles may integrate a wide spectrum of prooxidant signals via several mechanisms; the integration of such signals is, in turn, expressed as attenuated HDL antioxidative activity.

The absolute intrinsic antioxidative capacity of all small, dense HDL subfractions 3a, 3b, and 3c in protecting LDL from oxidation was significantly impaired in MetS patients. Such specific antioxidative activity was more potent in small, dense HDL3, compared with large, light HDL2, in both MetS subjects and controls, consistent with recent data obtained in healthy, normolipidemic subjects Furthermore, measurement of total antioxidative activity at equivalent plasma concentrations, i.

at the same 7-fold dilution for each HDL subfraction revealed that MetS HDL2a and 3a subfractions exerted diminished oxidative protection of LDL oxidation, compared with controls, thereby reflecting both attenuated intrinsic HDL antioxidative activity and lower particle concentrations.

Antioxidative activity of HDL can be expressed through multiple mechanisms 9. Removal and inactivation of lipid hydroperoxides LOOH , which accumulate during LDL oxidation, may however constitute the central mechanism accounting for HDL antioxidative properties Indeed, HDL-associated enzymes, including PON 10 , PAF-AH 11 , and lecithin:cholesterol acyltransferase 12 , may play a key role in the inactivation of LOOH by HDL.

In addition, apoA-I can prevent formation of oxidized lipids in LDL by removing seeding molecules of LOOH from LDL The impairment of HDL antioxidative capacity in MetS was selectively observed at late stages of LDL oxidation Fig.

LOOH removal and hydrolysis may underlie this effect. Of the HDL-associated enzymes possessing antioxidative activity, the activity of PON1, the major form of HDL-associated PON, was not decreased in MetS compared with controls Table 2. By contrast, PON1 activity was diminished in diabetic patients in previous studies 39 ; potentially, impaired glucose tolerance and more marked glycemia in diabetes, compared with MetS, may account for this difference We interpret these findings to indicate that neither PON1 nor PAF-AH can account for the impaired antioxidative activity of HDL subfractions in MetS.

Nonetheless, this interpretation does not entirely exclude a role for PON1 and PAF-AH in HDL antioxidative activity. Indeed, consistent with earlier data 14 , PON1 activity among HDL subfractions was functionally heterogeneous Table 2 ; and, in addition, dense HDL3c, which exhibited the highest PON1 activity against phenylacetate, possessed the most potent intrinsic antioxidative activity.

Moreover, we found a strong correlation between PON1 activity and HDL antioxidative capacity Fig. As documented earlier, the physicochemical properties and structural features of HDL subfractions may be implicated significantly in the expression of their antioxidative activity 14 , Consistent with studies in hypertriglyceridemic diabetic populations 43 , 44 , MetS HDL subfractions were enriched in TG and depleted in CE Table 2.

Such abnormalities are intimately linked to insulin resistance, hypertriglyceridemia, and excess adipose tissue, which is typical of both diabetic patients and nondiabetic MetS subjects. As a consequence of elevated release of fatty acids by adipose tissue and of the loss of insulin-mediated inhibition of hepatic TG-rich VLDL production, the liver overproduces VLDL Because lipoprotein lipase is less active in insulin resistant states 46 , the catabolism of VLDL is impaired.

As a consequence, an expanded plasma TG pool induces accelerated exchange of TG and CE between VLDL and other lipoproteins, including LDL and HDL. This process is mediated by CE transfer protein and results in the enrichment of TG and depletion of CE from both LDL and HDL particles. There are several possible hypotheses that might explain the impaired antioxidative activity of HDL subfractions in MetS.

Our present data support the hypothesis that abnormalities in physicochemical properties of HDL, and specifically TG enrichment of the core of HDL particles, underlie the impairment of the antioxidative properties of HDL subfractions.

This hypothesis is consistent with the positive correlation between the TG content of HDL subfractions and the rate of LDL oxidation in the propagation phase, as well as with the negative correlation between HDL TG content and the duration of this phase.

Mechanistically, the relationship between TG enrichment of HDL particles and impairment of antioxidative activity can be explained by the fact that HDL enrichment in TG considerably alters the conformation of the central and C-terminal domains of apoA-I 47 , which are critical for HDL to act as lipid acceptors More precisely, enrichment in TG reduces exposure of apoA-I to the aqueous phase due to its increased penetration into the lipid core of HDL 47 whose fluidity increases No difference was detected in apoA-I content of HDL subfractions between MetS patients and controls; we cannot exclude, however, the possibility that apoA-I function is altered in MetS.

Indeed, apoA-I may undergo oxidative modification in MetS subjects under elevated oxidative stress Table 1 ; moreover, MetS patients, even in the absence of diabetes, present moderately elevated plasma levels of glucose, which may favor glycation of apoA-I.

Such qualitative abnormalities of apoA-I are known to impair HDL antiatherogenic properties and, specifically, its capacity to accept lipids and to promote cellular cholesterol efflux 5 , Because apoA-I mediates removal of LOOH from LDL by HDL 13 , then this mechanism might lead to attenuated removal of oxidized lipids from LDL and tissues by HDL subfractions in MetS, and thus to impaired HDL antioxidative capacity.

In conclusion, these studies provide evidence that hypertriglyceridemia, hyperglycemia, and insulin resistance are closely linked to elevated systemic oxidative stress in MetS, which is, in turn, reflected in the impairment of HDL antioxidative properties. Therefore, our results imply that dysfunctional HDL subfractions play a central role in the expression of elevated oxidative stress in MetS.

Because oxidative stress is a key component of endothelial dysfunction, and thus of elevated CV risk in MetS, these results lead us to propose that early treatment of MetS patients, targeted at reduction of oxidative stress and normalization of HDL function, is necessary, even in the absence of diabetes.

Thus, thiazolidinediones, which can beneficially influence both insulin resistance and hyperinsulinemia 51 , or fibrates, which can selectively raise plasma levels of small, dense HDL3 containing apoA-I and apoA-II 52 , may prove efficacious in reducing oxidative stress and CV morbidity in MetS.

Because the potent antioxidative activity of HDL3, and especially HDL3c, is impaired to the highest degree in MetS, induction of selective increase in the circulating concentrations of these HDL subfractions may represent a new therapeutic approach for the attenuation of high CV risk in MetS subjects.

This work was supported by Association Claude Bernard to S. and by INSERM. is the recipient of a Research Fellowship from AstraZeneca, France.

is the recipient of a Research Fellowship from Nantes Centre Hospitaliere Universitaire. is the recipient of an INSERM Fellowship for Senior Investigators, a Fellowship from Fondation pour la Recherche Médicale, and an International High-Density Lipoprotein Research Award from Pfizer.

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J Lipid Res 41 : — gov website. Share sensitive information only on official, secure websites. Metabolic syndrome is the name for a group of risk factors for heart disease , diabetes , and other health problems.

You can have just one risk factor, but people often have several of them together. When you have at least three of them, it is called metabolic syndrome. These risk factors include:. The more factors you have, the higher your risk for heart disease, diabetes, and stroke is.

People who have metabolic syndrome often also have excessive blood clotting and inflammation throughout the body. Researchers don't know whether these conditions cause metabolic syndrome or worsen it. Most of the metabolic risk factors have no obvious signs or symptoms, except for a large waistline.

Your health care provider will diagnose metabolic syndrome based on the results of a physical exam and blood tests. You must have at least three of the risk factors to be diagnosed with metabolic syndrome:.

The most important treatment for metabolic syndrome is a heart-healthy lifestyle, which includes:. If making lifestyle changes is not enough, you may need to take medicines.

For example, you may need medicines to lower cholesterol or blood pressure. The information on this site should not be used as a substitute for professional medical care or advice. Contact a health care provider if you have questions about your health.

Metabolic Syndrome Also called: Insulin resistance syndrome, Metabolic syndrome X. On this page Basics Summary Start Here Symptoms. Learn More Related Issues Specifics. See, Play and Learn No links available.

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