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.

This relationship has been observed irrespective of age, blood pressure level, obesity, total cholesterol or LDL-cholesterol levels. Long-term follow-up of subjects with low HDL-cholesterol has demonstrated that their risk of developing CAD is similar to the risk in subjects with elevated total cholesterol or LDL-cholesterol.

Low HDL-cholesterol is the strongest predictor of subsequent cardiovascular events in patients with angiographically confirmed CAD and the levels of total cholesterol within normal range. According to current guidelines, the presence of low HDL-cholesterol should be considered a major cardiovascular risk factor which modifies the goal for LDL-lowering therapy and is used as a risk factor to estimate the year risk for CHD.

A low HDL-cholesterol level has several causes, some of which are associated with insulin resistance, i. elevated triglycerides, overweight and obesity, physical inactivity, and type 2 diabetes. The combination of a low HDL-cholesterol with elevated plasma triglyceride level has therefore been considered an insulin-resistant state.

It should be noted that certain drugs also reduce the level of HDL-cholesterol e. beta-blockers, anabolic steroids, progestational agents. Nevertheless, low HDL-cholesterol is an important component trait of metabolic syndrome and deserves close clinical attention and management since patients with this trait are at a high risk for CVD.

Similar conclusions have been reached in other study populations. The number and size of the HDL particles also play important roles in the risks of cardiovascular events in metabolic syndrome.

HDL molecules have demonstrated the most important role in the dyslipidemia, yet there are many unanswered questions: what regulates HDL concentration, subpopulations and functions? The cardioprotective function of HDL and the function of HDL concentration is unknown.

What is the relative contribution of cholesterol efflux, of antioxidant properties and the role of the anti-inflammatory characteristics of HDL subtypes? Further, there is no data to explain the relationship between overweight and smoking and low HDL.

Metabolic syndrome represents a clustering of cardiovascular risk factors linked through their association with insulin resistance Since insulin resistance is an independent risk factor for cardiovascular disease, its presence can lead to macrovascular complications long before other features of metabolic syndrome are evident.

It is very important to recognize that high LDL or high total cholesterol are not components of the metabolic syndrome.

In fact, LDL is often below average in patients with the metabolic syndrome. Thus, physicians must be aware that patients can still have a high risk of cardiovascular disease even if they have low LDL or total cholesterol. The incidence of metabolic syndrome has been increasing throughout Europe and North America, in parallel with an increase in overweight, obesity, and diabetes Since LDL has been emphasised in treatment guidelines quite effectively, it is now time to turn the attention of clinicians to metabolic syndrome.

If this epidemic of overweight and diabetes is not stopped, cardiovascular disease will increase and we will waste the progress we have made in the past 20 years. Metabolic syndrome requires a multi-factorial approach to treatment since all of its components combine to increase the risk of cardiovascular disease.

Firstly, diet and exercise will improve all components by lowering triglycerides, glucose and blood pressure, and raising HDL. Secondly, pharmacological therapy for improving the components of metabolic syndrome should be individualized in each patient. Challenges remaining in the identification of high-risk persons include the introduction of clinical markers of insulin resistance, integration of post challenge glucose and lipid concentrations, and better definition of the role of inflammatory, prothrombotic, and genetic factors Improved understanding of the risk factors for metabolic syndrome is required, and clinical trials of therapeutic interventions specifically targeted to this syndrome need to be conducted.

Notes Potential conflict of interest. References 1. Reaven GM. The metabolic syndrome: What is in a name? Clin Chem ; The metabolic syndrome or the insuline resistance syndrome?

Different names, different concepts, and different goals. Endorcinal Metab Clin N Am ;33; Third Report of the National Cholesterol Education Program NCEP Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults Adult Treatment Panel III final report.

Circulation ; Treatment of obesity: need to focus on high risk abdominally obese patients. BMJ ; Lamarche B, Tchernof A, Maurieége P, Cantin B, Dagenais GR, Lupien PJ, Despres JP. Fasting insulin and apolipoprotein B levels and low-density lipoprotein particle size as risk factors for ischemic heart disease.

JAMA ; Assmann G, Schulte H. Relation of high density lipoprotein cholesterol and triglycerides to incidence of atherosclerotic coronary artery disease the PROCAM experience Am J Cardiol. Mannienen V, Tekanen L, Koskinen P, Huttunen JK, Mänttäri M, Heinonen OP, Frick MH.

Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment. Donahue RP, Prineas RJ, Donahue RD, Zimmet P, Bean JA, De Courten M, et al.

Is fasting leptin associated with insulin resistance among nondiabetic individuals? Diabetes Care ; El Harchaoul K, van der Steeg WA, Stroes J, Kastelein J. Ronald Goldberg Miami, FL discussed LDL-targeted therapy, addressing the relationship between LDL cholesterol and CVD in diabetes, lessons learned from statin trials in diabetes, current guidelines for LDL-targeted therapy, and new data regarding the question of more rather than less statin, as well as special subgroups and obstacles to achieving goals.

In the UKPDS U. LDL particles enter the subendothelial space and are oxidized with subsequent uptake by macrophages, leading to their activation and to foam cell development, thereby beginning the process of atherosclerotic plaque development that leads to CVD events.

Additional factors associated with diabetes driving the atherosclerotic process include oxidative stress, inflammation, and cytokine excess, leading Goldberg to suggest an approach of LDL lowering for persons with diabetes beyond the degree required in nondiabetic persons.

An important question is the appropriate intensity of statin treatment. In the REVERSAL Reversal of Atherosclerosis with Aggressive Lipid Lowering trial, intravascular ultrasound was used to study coronary artery plaque progression following an month period of treatment with 40 mg pravastatin versus 80 mg atorvastatin daily in persons with CHD, showing 2.

In the HPS, persons who appeared to have type 1 diabetes showed evidence of parallel benefit from statin therapy, and there is evidence that CVD in persons with type 1 diabetes begins around age 40 years, suggesting that statins should be initiated by age 30 in this group 6.

Similarly, younger persons with type 2 diabetes have more markedly increased relative CVD risk than older type 2 diabetic persons 7 , implying that early initiation of statins is appropriate for all young persons with diabetes when LDL levels are even mildly elevated.

Another important group is that of persons with renal insufficiency. In the HPS, there were diabetic persons with elevated creatinine; the event rate was almost twice that of those with normal creatinine levels, suggesting this to be a group particularly benefiting from treatment.

Several studies presented at the meeting reviewed effects of ezetimibe. Denke et al. abstract reported the effect of addition of ezetimibe to statin therapy. In a small study, Wolf and King abstract compared 61 diabetic subjects given a double dose of atorvastatin dose with 25 subjects who were also given ezitimibe.

The results showed a 20 vs. McKenney et al. abstract reported the effects of 20 mg simvastatin alone vs. Helen Colhoun London, U. and Ireland to address the role of lipid lowering with 10 mg atorvastatin daily versus placebo in 2, 1, vs.

Comparing the placebo and atorvastatin groups, there were vs. There were vs. Fatal and nonfatal myocardial infarction occurred in 20 vs. Death occurred in 82 vs. Colhoun concluded that statin treatment is safe and efficacious, suggesting that there is no justification for an LDL threshold, but rather that overall CVD risk should be the determining factor in which patients should receive this treatment, leading to the question as to whether any patients with type 2 diabetes are at sufficiently low risk that statins should not be used.

Arthur Charles Tustin, CA discussed HDL-targeted therapy, reviewing the function of HDL and the effects of various treatment approaches. Low HDL cholesterol is the most common lipid abnormality, underlying CHD, metabolic syndrome, and dysglycemia, with additive adverse effect to elevations in LDL.

Although niacin is not widely used clinically, there has been evidence of benefit of treatment with this agent for more than a decade. HDL is comprised of a heterogeneous set of molecules, mediating reverse cholesterol transport, involving proteins including apoA1, lecithin-cholesterol acyl transferase LCAT , cholesterol ester transfer protein CETP , and ATP-binding cassette transporter A1.

HDL has antioxidant effects mediated by apoA1, paraoxonases, LCAT, and platelet-activating factor; anti-inflammatory effects, in part by blocking adhesion of monocytes; endothelium-stabilizing effects by promoting nitric oxide NO synthesis, and actions reducing platelet aggregation and promoting fibrinolysis.

Nascent HDL particles contain two apoA1 molecules, phospholipids and triglycerides, and attach to tissues that express ATP-binding cassette transporter A1, gaining free cholesterol. In the presence of LCAT, HDL cholesterol can be esterified, producing larger molecules that may be subsequently modified by paraoxonases.

CETP interacts with this particle and with LDL and VLDL1 particles, with cholesterol ester transferring to LDL particles both directly and indirectly via VLDL. Cholesterol ester from HDL is taken up by the liver directly by hepatic HDL holoparticle receptors and indirectly via the LDL receptor and by scavenger receptor class B, type I, with cholesterol ester then excreted in bile.

In persons with type 2 diabetes, there are increased levels of VLDL1, with its triglycerides being taken up by HDL2 particles, which are then hydrolyzed via hepatic lipase, and the smaller HDL particles then potentially excreted in the urine. CETP also can transfer triglycerides from VLDL via lipoprotein lipase LPL to an LDL subspecies that is acted on by hepatic lipase to produce small dense LDL SD-LDL particles.

Charles discussed a variety of approaches to monotherapy and combination treatment of low HDL cholesterol for persons with diabetes Table 1. Statins may increase HDL2 levels and reduce SD-LDL, and combination fenofibrate-statin treatment markedly decreases apoB.

LDL size itself, Charles stated, is misleading, with the SD-LDL cholesterol mass a better therapeutic target. Niacin increases LDL size, for example, while statins lower LDL mass, so that combined use of both has optimal effect. Overall, he stated, HbA 1c levels improved.

In a related open-label analysis of diabetic patients in his clinic, niacin mean dose 2. Hypertriglyceridemia can cause chylomicron-related pancreatitis, the likelihood of which is decreased by lowering dietary fat and simple sugars with use of low—glycemic index foods, avoidance of alcohol, and avoidance of medications such as corticosteroids, β-blockers, and high-dose thiazides; by improving glycemia; and by using triglyceride-lowering drugs.

Triglyceride lowering for CVD risk treatment is more complex. Triglycerides may be markers for atherogenic triglyceride-rich particles, including intermediate-density lipoproteins and remnant particles, which may directly lead to formation of foam cells, to atherosclerotic lesions, and to unstable plaques.

Triglycerides are also associated with other lipoprotein abnormalities, such as SD-LDL, low levels of HDL, and elevations in non-HDL cholesterol and apoB, and with hypercoagulability, endothelial dysfunction, decreased fibrinolysis, and a proinflammatory state A meta-analysis has confirmed and extended these individual study findings There is evidence that CVD is associated with postprandial triglyceride elevation even after adjustment for fasting levels.

Certain genetic polymorphisms are associated with triglyceride elevations and increased CVD risk, showing interaction with environmental factors. Thus, persons with the apoE4 allele have particular risk with cigarette use, as do those with the apoC-III promoter polymorphism who have the metabolic syndrome, those with the LPL polymorphism who are obese, and persons with polymorphisms of fatty acid binding protein 2 who have diabetes.

Briefly reviewing treatment, Georgopoulos noted that three fibrate trials, DIAS Diabetes Atherosclerosis Intervention Study 24 , Veterans Affairs High-Density Lipoprotein Intervention Trial VA-HIT 25 , and Helsinki 26 showed benefit of treatment with fenofibrate and gemfibrozil, although the Benzafibrate Infarction Prevention study failed to show benefit with bezafibrate treatment.

Combination treatment with atorvastatin plus rosiglitazone may be particularly effective in reducing triglycerides, and there is evidence that simvastatin plus niacin both lowers triglycerides and reduces atherosclerosis Lifestyle approaches, including exercise, cigarette discontinuation, weight loss, and fish intake also reduce triglycerides and CVD risk.

Thus, although all these approaches to treatment also affect other lipoproteins and other CVD risk factors, there is suggestive evidence of benefit of triglyceride-targeted therapy.

In a study presented at the meeting, Altomonte et al. abstract studied the mechanism of action of fibrates, showing evidence that the nuclear Forkhead transcription factor Foxo1, suppression of which mediates aspects of insulin action, is also suppressed by fibrates in a high fructose—fed Syrian golden hamster model.

Thus, under circumstances of resistance to the inhibitory effect of insulin on hepatic production of apoC-III and hence triglyceride-containing lipoproteins, fibrates may have insulin-sensitizing effects, contributing to decreased apoC-III production and improved triglyceride metabolism in subjects with diabetic dyslipidemia.

Dardik et al. Hirano abstract reported the use of the angiotensin II receptor blocker olmesartan in insulin-resistant versus control rats, showing blood pressure lowering in both but improvement in insulin sensitivity, lowering of fasting glucose, and reduction in hepatic triglycerides levels only in the insulin-resistant animals, suggesting that blockade of angiotensin action may decrease triglyceride production independent of effects on blood pressure.

Drexel et al. abstract prospectively followed persons with angiogram-proven coronary disease, of whom had type 2 diabetes, showing the latter group to have association of a composite factor based on triglycerides, HDL, and apoA1 but not of a factor based on LDL cholesterol and apoB with vascular end points during a 2.

Chu et al. Betteridge and Gibson abstract compared the effects of rosuvastatin with atorvastatin in patients with type 2 diabetes. Non-HDL cholesterol decreased 45 vs. Triglyceride-rich lipoproteins as a causal factor for cardiovascular disease. Vasc Health Risk Manag 12 , — Leroux, G.

Influence of triglyceride concentration on the relationship between lipoprotein cholesterol and apolipoprotein B and A-I levels. Metabolism 49 , 53—61 Srisawasdi, P. Estimation of plasma small dense LDL cholesterol from classic lipid measures.

Am J Clin Pathol , 20—29 Barter, P. Cholesteryl ester transfer protein: a novel target for raising HDL and inhibiting atherosclerosis. Wilkins, J. Discordance Between Apolipoprotein B and LDL-Cholesterol in Young Adults Predicts Coronary Artery Calcification: The CARDIA Study.

J Am Coll Cardiol 67 , — Download references. Sílvia Cristina de Sousa Paredes. Endocrinology Department, Hospital de Braga, Sete Fontes, São Victor, , Braga, Portugal.

Liliana Cecília Martins da Fonseca. Endocrinology Department, Centro Hospitalar e Universitário do Porto, Largo Professor Abel Salazar, , Porto, Portugal. Laura Virgínia Pereira Teixeira Ribeiro. Department of Public Health and Forensic Sciences, and Medical Education, Medical Education Unit, Faculty of Medicine of the University of Porto, , Porto, Portugal.

I3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, , Porto, Portugal. Maria Helena da Silva Ramos. José Carlos Azevedo Oliveira. Clinical Chemistry Department, Centro Hospitalar e Universitário do Porto, Largo Professor Abel Salazar, , Porto, Portugal. Isabel Maria Gonçalves Mangas Neto da Palma.

You can also search for this author in PubMed Google Scholar. and I. designed the study; S. and L. acquired the data; S. did the data analysis; S. interpreted the data; S. drafted the work and all authors revised it critically for important intellectual content.

All authors approved the final version submitted and are accountable for all aspects of the work. All authors read and approved the final manuscript. Correspondence to Sílvia Paredes. Open Access This article is licensed under a Creative Commons Attribution 4.

Reprints and permissions. Paredes, S. Novel and traditional lipid profiles in Metabolic Syndrome reveal a high atherogenicity.

Sci Rep 9 , Download citation. Received : 25 January Accepted : 04 July Published : 13 August 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.

International Journal of Diabetes in Developing Countries Environmental Science and Pollution Research By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily. Skip to main content Thank you for visiting nature. nature scientific reports articles article.

Download PDF. Subjects Dyslipidaemias Metabolic syndrome. Abstract Low-density-lipoprotein cholesterol LDL-c guides lipid-lowering therapy, although other lipid parameters could better reflect cardiovascular disease CVD risk. Introduction The importance of low-density lipoprotein LDL cholesterol LDL-c reduction to prevent cardiovascular CV disease CVD is strongly acknowledged 1 , 2.

Laboratory analysis Biochemical laboratory tests were conducted after an 8-hour night fast. Statistical analysis Statistical analysis was performed using IBM SPSS® version Table 1 Comparison of clinical and laboratory variables between MetS patients with LDL-c within and above target.

Full size table. Table 2 Comparison of lipid profile between MetS patients with LDL-c within and above target. Table 3 Predictors of LDL-c within target. Discussion As CVD is the most common cause of death in the developed world 12 , early identification of individuals at increased CV risk is a priority.

Lp a and small and dense LDL particles Lp a is an independent risk factor for CVD 3 as well as in MetS individuals Lipid parameters correlations As stated before, concomitant dyslipidemia has a particular pattern characterized by a high flux of free fatty acids, hypertriglyceridemia, low HDL-c values, increased sd-LDL particles and high ApoB values 36 , Limitations Our study has some limitations.

Summary Our study also has strengths. Conclusions LDL-c reduction has long been the major goal of lipid-modulating therapies; however, patients continue to exhibit CVD-related events.

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Article CAS Google Scholar Download references. Author information Authors and Affiliations Sílvia Cristina de Sousa Paredes. Endocrinology Department, Hospital de Braga, Sete Fontes, São Victor, , Braga, Portugal Sílvia Paredes Liliana Cecília Martins da Fonseca.

Endocrinology Department, Centro Hospitalar e Universitário do Porto, Largo Professor Abel Salazar, , Porto, Portugal Liliana Fonseca Laura Virgínia Pereira Teixeira Ribeiro.

Department of Public Health and Forensic Sciences, and Medical Education, Medical Education Unit, Faculty of Medicine of the University of Porto, , Porto, Portugal Laura Ribeiro I3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, , Porto, Portugal Laura Ribeiro Maria Helena da Silva Ramos.

Endocrinology Department, Centro Hospitalar e Universitário do Porto, Largo Professor Abel Salazar, , Porto, Portugal Helena Ramos José Carlos Azevedo Oliveira.

Clinical Chemistry Department, Centro Hospitalar e Universitário do Porto, Largo Professor Abel Salazar, , Porto, Portugal José Carlos Oliveira Isabel Maria Gonçalves Mangas Neto da Palma.

Endocrinology Department, Centro Hospitalar e Universitário do Porto, Largo Professor Abel Salazar, , Porto, Portugal Isabel Palma Authors Sílvia Paredes View author publications. View author publications. Ethics declarations Competing Interests The authors declare no competing interests.

Rights and permissions Open Access This article is licensed under a Creative Commons Attribution 4. About this article. Cite this article Paredes, S. Copy to clipboard. Khandagale Vinesh S. Kamble Satyajeet P. Khare International Journal of Diabetes in Developing Countries Value of the triglyceride—glucose index and non-traditional blood lipid parameters in predicting metabolic syndrome in women with polycystic ovary syndrome Lijuan Zhang Hui Wang Liuliu Ren Hormones Genetic or therapeutic neutralization of ALK1 reduces LDL transcytosis and atherosclerosis in mice Sungwoon Lee Hubertus Schleer William C.

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Influence of triglyceride concentration on the relationship between lipoprotein cholesterol and apolipoprotein B and A-I levels.

Metabolism 49 , 53—61 Srisawasdi, P. Estimation of plasma small dense LDL cholesterol from classic lipid measures. Am J Clin Pathol , 20—29 Barter, P. Cholesteryl ester transfer protein: a novel target for raising HDL and inhibiting atherosclerosis.

Wilkins, J. Discordance Between Apolipoprotein B and LDL-Cholesterol in Young Adults Predicts Coronary Artery Calcification: The CARDIA Study. J Am Coll Cardiol 67 , — Download references. Sílvia Cristina de Sousa Paredes. Endocrinology Department, Hospital de Braga, Sete Fontes, São Victor, , Braga, Portugal.

Liliana Cecília Martins da Fonseca. Endocrinology Department, Centro Hospitalar e Universitário do Porto, Largo Professor Abel Salazar, , Porto, Portugal. Laura Virgínia Pereira Teixeira Ribeiro.

Department of Public Health and Forensic Sciences, and Medical Education, Medical Education Unit, Faculty of Medicine of the University of Porto, , Porto, Portugal. I3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, , Porto, Portugal.

Maria Helena da Silva Ramos. José Carlos Azevedo Oliveira. Clinical Chemistry Department, Centro Hospitalar e Universitário do Porto, Largo Professor Abel Salazar, , Porto, Portugal. Isabel Maria Gonçalves Mangas Neto da Palma. You can also search for this author in PubMed Google Scholar.

and I. designed the study; S. and L. acquired the data; S. did the data analysis; S. interpreted the data; S. drafted the work and all authors revised it critically for important intellectual content. All authors approved the final version submitted and are accountable for all aspects of the work.

All authors read and approved the final manuscript. Correspondence to Sílvia Paredes. Open Access This article is licensed under a Creative Commons Attribution 4. Reprints and permissions. Paredes, S. Novel and traditional lipid profiles in Metabolic Syndrome reveal a high atherogenicity.

Sci Rep 9 , Download citation. Received : 25 January Accepted : 04 July Published : 13 August 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. International Journal of Diabetes in Developing Countries Environmental Science and Pollution Research By submitting a comment you agree to abide by our Terms and Community Guidelines.

If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate. Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily. Skip to main content Thank you for visiting nature.

nature scientific reports articles article. Download PDF. Subjects Dyslipidaemias Metabolic syndrome. Abstract Low-density-lipoprotein cholesterol LDL-c guides lipid-lowering therapy, although other lipid parameters could better reflect cardiovascular disease CVD risk.

Introduction The importance of low-density lipoprotein LDL cholesterol LDL-c reduction to prevent cardiovascular CV disease CVD is strongly acknowledged 1 , 2. Laboratory analysis Biochemical laboratory tests were conducted after an 8-hour night fast. Statistical analysis Statistical analysis was performed using IBM SPSS® version Table 1 Comparison of clinical and laboratory variables between MetS patients with LDL-c within and above target.

Full size table. Table 2 Comparison of lipid profile between MetS patients with LDL-c within and above target.

Table 3 Predictors of LDL-c within target. Discussion As CVD is the most common cause of death in the developed world 12 , early identification of individuals at increased CV risk is a priority.

Lp a and small and dense LDL particles Lp a is an independent risk factor for CVD 3 as well as in MetS individuals Lipid parameters correlations As stated before, concomitant dyslipidemia has a particular pattern characterized by a high flux of free fatty acids, hypertriglyceridemia, low HDL-c values, increased sd-LDL particles and high ApoB values 36 , Limitations Our study has some limitations.

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Dyslipidemia in chronic kidney disease: an approach to pathogenesis and treatment. J Am Soc Nephrol. Download references. We thank all of the study participants. We also are thankful to the Research Undersecretary of Tabriz University of Medical Sciences for their financial support.

The present study has been financially supported by a grant from Tabriz University of Medical Sciences. Code: IR. The funders had no role in hypothesis generation, recruiting and designing the study.

Their role was only financial supporting. Department of Internal Medicine, Faculty of Medical Science, Mazandaran University of Medical Science, Sari, Iran. Medical Physiology, Basic Sciences Department, College of Pharmacy, University of Duhok, Kurdistan, Iraq.

Isfahan Kidney Diseases Research Center, School of Medicine, Khorshid Hospital, Isfahan University of Medical Sciences, Isfahan, Iran. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.

Department of Internal Medicine, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran. You can also search for this author in PubMed Google Scholar. ZHN and BAZ were involved in data collection and manuscript writing. ZHN also conceptualized the first hypothesis of work and was also involved in writing the first draft of the paper.

SV, ALJ and ZH were involved in data collection and analysis. ALJ also performed the lab works. Correspondence to Azam Mivefroshan. This study protocol has been approved by the ethics committee of the Tabriz University of Medical Sciences, Code: IR.

Written informed consent was obtained from all of the participants before participation in the study. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is licensed under a Creative Commons Attribution 4.

Reprints and permissions. Ardekani, A. et al. The association between lipid profile, oxidized LDL and the components of metabolic syndrome with serum mineral status and kidney function in individuals with obesity.

BMC Res Notes 16 , Download citation. Received : 25 December Accepted : 23 August Published : 05 September 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 Metabolic syndrome MetS is presented with a cluster of cardio-metabolic risk factors with widespread prevalence.

Methods This study included individuals with obesity of both gender with or without MetS as the case and control, respectively. Conclusion Our results suggest that disturbed serum lipids in obesity-metabolic syndrome is associated with homeostatic changes in the level of minerals or proteins that are involved in their metabolism.

Background Metabolic syndrome MetS is characterized by various risk factors such as hypertension, central obesity, glucose intolerance, insulin resistance IR , and dyslipidemia [ 1 , 2 , 3 ].

Materials and methods Study design This case-control study included 62 individuals with obesity and MetS and 65 individuals with obesity and without MetS from August to October Anthropometric measurements Body weight was measured at fasting state by calibrated Seca scale Dubai, United Arab Emirates with light clothes and without shoes and an accuracy of g, and height was measured using stadiometer at approximately 0.

Appetite measurements The Visual Analogue Scale VAS was used for appetite assessments. Biochemical assessments and blood pressure In this study, 5 ml of fasting blood samples were collected from all participants after 12—14 h of fasting.

Statistical analyses SPSS software version 24, SPSS Inc. Results The present study included individuals with obesity 62 with MetS and 65 without MetS.

The results are as follows : Demographic findings of the study subgroups Demographic information of the participants is provided in Table 1. Table 1 The baseline characteristics of the study subjects Full size table.

Table 2 The comparison of biochemical parameters among study groups Full size table. Table 3 The correlation between magnesium, copper, calcium, phosphorous, and iron with components of metabolic syndrome in study groups Full size table.

Table 4 The correlation between total protein, albumin, urea, creatinine, and uric acid with the components of metabolic syndrome in study groups Full size table. Discussion In the current study, we evaluated the association between metabolic risk factors, including Ox-LDL, lipid profile and components of MetS with mineral status and renal function tests among individuals with obesity and with or without MetS.

Limitations of the current study This study has some limitations; first of all, the assessment of renal function tests was limited, and no information on GFR, and blood electrolytes was available. Future directions Further longitudinal studies are required to infer the causality. Abbreviations ATP III: Adult Treatment Panel III BMI: Body mass index CAD: Coronary artery disease CHD: Coronary heart disease CKD: Chronic kidney disease DBP: Diastolic blood pressure ELISA: Enzyme-linked immunosorbent assay FBS: Fasting blood glucose GFR: Glomerular filtration rate HDL: High density lipoprotein cholesterol LDL: Low density lipoprotein cholesterol MetS: Metabolic syndrome SBP: Systolic blood pressure T2DM: Type 2 diabetes mellitus TC: Total cholesterol TG: Triglyceride VAS: Visual Analogue Scale WC: Waist circumference.

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Eur Heart J. Download references. For this study we acknowledge the contributions of the general practitioners, midwives, pharmacies, the Municipal Health Service in the area Rotterdam, hospitals in Rotterdam, the Stichting Trombosedienst and Artsenlaboratorium Rijnmond and the participation of all participants.

The Erasmus Medical Centre conduct the Generation R study in close collaboration with the School of Law and the Faculty of Social Sciences of the Erasmus University.

The financial support for the Generation R study was made possible by the Erasmus Medical Centre, Erasmus University Rotterdam and the Netherlands Organization for Health Research and Development, the Netherlands Organization for Scientific Research, the Ministry of Health, Welfare and Sport, and the Ministry of Youth and Families.

Department of Obstetrics and Gynaecology, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, the Netherlands.

Maria C. Adank, Laura Benschop, Sophia P. van Streun, Anna M. Smak Gregoor, Eric A. Generation R Study Group, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands. Department of General Medicine, Erasmus MC, University Medical Centre Rotterdam, PO Box , CA, Rotterdam, The Netherlands.

Monique T. Roeters van Lennep. You can also search for this author in PubMed Google Scholar. MC Adank analyzed the data and wrote the article. L Benschop, SP van Streun and AM Smak Gregoor contributed to the design of the paper, analyses and assisted with writing of the article.

MT Mulder, EAP Steegers, S Schalekamp-Timmermans and JE Roeters van Lennep contributed to the design of the paper, writing of the article, interpretation of the data, revisions and gave input at all stages of the study.

The authors read and approved the final manuscript. Correspondence to Jeanine E. Written consent was obtained from all participants. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Table S2. Baseline characteristics of women with and without available lipid measurements six years after pregnancy. Open Access This article is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material.

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Adank, M. et al. Gestational lipid profile as an early marker of metabolic syndrome in later life: a population-based prospective cohort study. BMC Med 18 , Download citation. Received : 06 October Accepted : 23 November Published : 23 December Anyone you share the following link with will be able to read this content:.

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Dyslipidemia in chronic kidney disease: an approach to pathogenesis and treatment. J Am Soc Nephrol. Download references. We thank all of the study participants.

We also are thankful to the Research Undersecretary of Tabriz University of Medical Sciences for their financial support. The present study has been financially supported by a grant from Tabriz University of Medical Sciences.

Code: IR. The funders had no role in hypothesis generation, recruiting and designing the study. Their role was only financial supporting. Department of Internal Medicine, Faculty of Medical Science, Mazandaran University of Medical Science, Sari, Iran.

Medical Physiology, Basic Sciences Department, College of Pharmacy, University of Duhok, Kurdistan, Iraq. Isfahan Kidney Diseases Research Center, School of Medicine, Khorshid Hospital, Isfahan University of Medical Sciences, Isfahan, Iran.

Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran. Department of Internal Medicine, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran. You can also search for this author in PubMed Google Scholar. ZHN and BAZ were involved in data collection and manuscript writing.

ZHN also conceptualized the first hypothesis of work and was also involved in writing the first draft of the paper. SV, ALJ and ZH were involved in data collection and analysis. ALJ also performed the lab works. Correspondence to Azam Mivefroshan. This study protocol has been approved by the ethics committee of the Tabriz University of Medical Sciences, Code: IR.

Written informed consent was obtained from all of the participants before participation in the study. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Open Access This article is licensed under a Creative Commons Attribution 4. Reprints and permissions. Ardekani, A. et al. The association between lipid profile, oxidized LDL and the components of metabolic syndrome with serum mineral status and kidney function in individuals with obesity.

BMC Res Notes 16 , Download citation. Received : 25 December Accepted : 23 August Published : 05 September 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 Metabolic syndrome MetS is presented with a cluster of cardio-metabolic risk factors with widespread prevalence.

Methods This study included individuals with obesity of both gender with or without MetS as the case and control, respectively. Conclusion Our results suggest that disturbed serum lipids in obesity-metabolic syndrome is associated with homeostatic changes in the level of minerals or proteins that are involved in their metabolism.

Background Metabolic syndrome MetS is characterized by various risk factors such as hypertension, central obesity, glucose intolerance, insulin resistance IR , and dyslipidemia [ 1 , 2 , 3 ]. Materials and methods Study design This case-control study included 62 individuals with obesity and MetS and 65 individuals with obesity and without MetS from August to October Anthropometric measurements Body weight was measured at fasting state by calibrated Seca scale Dubai, United Arab Emirates with light clothes and without shoes and an accuracy of g, and height was measured using stadiometer at approximately 0.

Appetite measurements The Visual Analogue Scale VAS was used for appetite assessments. Biochemical assessments and blood pressure In this study, 5 ml of fasting blood samples were collected from all participants after 12—14 h of fasting.

Statistical analyses SPSS software version 24, SPSS Inc. Results The present study included individuals with obesity 62 with MetS and 65 without MetS. The results are as follows : Demographic findings of the study subgroups Demographic information of the participants is provided in Table 1.

Table 1 The baseline characteristics of the study subjects Full size table. Table 2 The comparison of biochemical parameters among study groups Full size table. Table 3 The correlation between magnesium, copper, calcium, phosphorous, and iron with components of metabolic syndrome in study groups Full size table.

Table 4 The correlation between total protein, albumin, urea, creatinine, and uric acid with the components of metabolic syndrome in study groups Full size table. Discussion In the current study, we evaluated the association between metabolic risk factors, including Ox-LDL, lipid profile and components of MetS with mineral status and renal function tests among individuals with obesity and with or without MetS.

Limitations of the current study This study has some limitations; first of all, the assessment of renal function tests was limited, and no information on GFR, and blood electrolytes was available.

Future directions Further longitudinal studies are required to infer the causality. Abbreviations ATP III: Adult Treatment Panel III BMI: Body mass index CAD: Coronary artery disease CHD: Coronary heart disease CKD: Chronic kidney disease DBP: Diastolic blood pressure ELISA: Enzyme-linked immunosorbent assay FBS: Fasting blood glucose GFR: Glomerular filtration rate HDL: High density lipoprotein cholesterol LDL: Low density lipoprotein cholesterol MetS: Metabolic syndrome SBP: Systolic blood pressure T2DM: Type 2 diabetes mellitus TC: Total cholesterol TG: Triglyceride VAS: Visual Analogue Scale WC: Waist circumference.

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To assess whether the association of lipid levels in early pregnancy and metabolic syndrome was stronger in women with higher concentrations of lipid levels total cholesterol, triglycerides, LDL-c, remnant cholesterol and non-HDL-c in early pregnancy and respectively lower levels of HDL-c, lipid levels in early pregnancy were categorized as quartiles and subsequently used as a categorical measure Fig.

Confounders that were included in the regression models were selected based on their associations with the exposure and outcomes of interest and based on previous studies. The selected confounders included: maternal age at intake, gestational age at blood sampling, educational level, ethnicity, parity, smoking, and folic acid supplementation.

For the association of gestational lipid levels with lipid levels six years after pregnancy, pre-pregnancy BMI was additionally added to the regression models. In attempt to exclude the effect of placental syndromes, we examined the incidence of metabolic syndrome in this subgroup of women and repeated all the analyses excluding women with a placental syndrome in their index pregnancy Fig.

Statistical analyses were performed using the IBM Statistical Package of Social Sciences version Presented data are adjusted for maternal age, gestational age at blood sampling, ethnicity, educational level, parity, smoking, and folic acid supplementation.

Abbreviations: OR, odds ratio; CI, confidence interval; Q, quartile; LDL-c, low-density lipoprotein cholesterol; HDL-c, high-density lipoprotein cholesterol. Characteristics of participants with and without metabolic syndrome. Metabolic syndrome according to the ATP III Diagnostic criteria.

Metabolic syndrome is stratified by its components. For each component, the valid percentages of participants with and without metabolic syndrome are presented. Abbreviations: HDL-c, high-density lipoprotein cholesterol. This study included a total of women Table 1.

Women were on average Total cholesterol, triglycerides, LDL-c, HDL-c, remnant cholesterol and non-HDL-c levels were positively associated with their corresponding lipid level six years after pregnancy Additional file 1 : Table S1.

These associations were independent of pre-pregnancy BMI. Six years after pregnancy, Table 3 shows the association between maternal lipid levels in early pregnancy with metabolic syndrome six years after pregnancy. Women with higher levels of total cholesterol, triglycerides, LDL-c, remnant cholesterol and non-HDL-c levels in early pregnancy were more at risk of developing metabolic syndrome six years after pregnancy.

These associations remained statistically significant after adjustment for confounders. HDL-c was negatively and independently associated with metabolic syndrome. Figure 2 shows that compared to total cholesterol and LDL-c levels in the lower quartile, those in the highest quartile were associated with an increased risk of metabolic syndrome OR 2.

Compared to HDL-c levels in the highest quartile, those in the lower quartiles were associated with an increased risk of metabolic syndrome, with the highest risk for women in the lowest quartile OR 7. Women with triglyceride and remnant cholesterol levels in the highest quartile had the highest risk of metabolic syndrome OR Compared to non-HDL-c levels in the lowest quartile, early pregnancy non-HDL-c levels in the third and fourth quartile were associated with an increased risk of metabolic syndrome, with the highest risk for women in the highest quartile OR 4.

The most common feature of metabolic syndrome was low HDL-c Of the women without a placental syndrome in their index pregnancy, 8. The prevalence of individual MS components were comparable to those of the total population: low-HDL-c Of the women with a placental syndrome in their index pregnancy, 71 Their most common feature of metabolic syndrome was also low HDL-c Women with a placental syndrome had a higher risk OR 1.

This study shows that lipid levels in early pregnancy are positively associated with lipid levels and the prevalence of metabolic syndrome six years after pregnancy.

These associations remained significant after correction for smoking and BMI. Previous studies on lipid levels measured in pregnancy and later in life are mostly limited to measurements up to one year postpartum [ 16 , 17 , 32 ].

These studies show that lipid levels initially decrease in pregnancy followed by a gradual increase and peak at the end of the third trimester.

Lipid levels decline to plateau at four months after the delivery [ 18 ]. Postpartum total cholesterol levels and LDL-c levels remain somewhat but are significantly higher than the levels measured before pregnancy. However, these studies do not report on the association of gestational lipid levels with lipid levels after pregnancy.

A previous study performed within the Generation R study population found that lipid levels in early pregnancy increase moderately with advancing gestational age in the time-frame when lipids in this study were measured [ 20 ].

Results from this study show that lipid levels measured in early pregnancy may already be indicative for lipid levels six years later, independent of smoking and BMI. Since early pregnancy lipid levels are also associated with adverse pregnancy outcomes and blood pressure during and after pregnancy [ 20 ], measurement of lipid levels in early pregnancy may improve short and long-term health of women.

The prevalence of metabolic syndrome in our relatively young and highly educated population of women was Data on prevalence of metabolic syndrome in young women is scarce.

A possible explanation may be that their mean BMI was higher and that their educational level was lower which is associated with an increased risk of metabolic syndrome [ 34 ]. Previous studies assessed the prevalence of metabolic syndrome in women who experienced hypertensive disorders of pregnancy, however almost all of these studies lacked a control group.

Within these populations some found that women with early-onset pre-eclampsia had a higher risk of developing metabolic syndrome [ 8 ], whereas others did not find such an association [ 35 ]. A Canadian study, consisting of women, found that the prevalence of metabolic syndrome after one and three years after pregnancy was The mean BMI in that study was higher compared to that in our study We hypothesized that BMI would be the main risk factor driving the association between gestational lipids and the lipid profile six years after pregnancy.

However, these associations remained significant also after adjusting for pre-pregnancy BMI. Lipid levels are partially determined by lifestyle factors, but also by genetics [ 37 , 38 ]. Several other studies also found that genetic background has a large influence on lipid concentrations which may be the reason why these associations remain significant after adjusting for BMI [ 38 , 39 , 40 ].

This is interesting since it suggests that lipid levels have a certain level of stability; independent of lifestyle factors. Therefore, unfavorable lipid levels may be an early marker for future cardiovascular risk.

In our population the majority of women remained in the same quartile in pregnancy and six years after pregnancy data not shown , supporting this hypothesis. As shown in previous studies, women with a placental syndrome have an increased risk of metabolic syndrome and CVD later in life [ 41 ].

Therefore, we performed the same analyses in a subset of women without placental syndromes. This did not affect our results. We therefore hypothesize that our results may be explained by genetic inheritance and to a lesser extent by lifestyle or pregnancy-related factors.

Unfortunately, the nature of our study did not allow further investigation of this genetic contribution. In young, fertile women monitoring of lipid levels may be relevant due to the association with CVD later in life.

Currently, guidelines of the American Heart Association and guidelines of the European Society of Cardiology do not advice to determine gestational lipid levels [ 42 , 43 ].

However, in our opinion adding lipids to the routine blood measurements in early pregnancy may provide an opportunity to early identify women with an increased CVD risk profile.

This may be beneficial for timely intervention and prevention of metabolic syndrome and subsequently possible CVD in later life.

Especially as women are more prone to improve lifestyle during pregnancy [ 44 ]. Strengths of our study are the prospective and structured data collection from early pregnancy onwards.

We also have a large sample of women with blood samples six years after pregnancy available. Some limitations need to be considered. First, blood samples were obtained in a non-fasting state. However, according to the joint consensus statement from the European Atherosclerosis Society and the European Federation of Clinical Chemistry and Laboratory Medicine lipids and lipoproteins change minimally in response to normal food intake [ 45 ].

Second, pre-pregnancy BMI was self-reported. Nevertheless, pre-pregnancy BMI was strongly correlated with BMI measured in early pregnancy, which makes misclassification unlikely. Third, waist circumference was only measured ten years after pregnancy.

Therefore, we assumed that waist circumference ten years after pregnancy could be used as a proxy for waist circumference six years after pregnancy. Finally, similar to other studies, the non-response six years after pregnancy may have led to selection of relatively healthy women, which may affect the generalizability of results to high-risk populations Additional file 1 : Table S2.

The gestational lipid profile is associated with the lipid profile and metabolic syndrome six years after pregnancy, independent of smoking and BMI. Having a more atherogenic gestational lipid profile may act as an early risk marker for CVD later in life.

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