Dense Low-density Lipoprotein Particles Research Articles

Effect of oral vitamin E supplementation on lipid profile in diabetes mellitus: evidence based case report

Introduction: Diabetes mellitus, a prominent non-communicable disease, presents as a chronic condition associated with various complications, including heart disease, nerve damage, chronic kidney disease, and dyslipidemia. A pivotal abnormality in diabetic dyslipidemia is insulin resistance, which stimulates the production of Hepatic VLDL1 (very-low-density lipoprotein 1). The resulting overproduction of VLDL1 is metabolically linked to an abundance of small, dense LDL (low-density lipoprotein) particles and a reduction in large, cholesterol-rich HDL2 (high-density lipoprotein). Conversely, vitamin E, known for its antioxidant and anti-inflammatory properties, acts as a remover of peroxyl radicals, preventing lipid oxidation and safeguarding polyunsaturated fatty acids (PUFA) within cells and plasma lipoproteins.
 Method: This study investigates the impact of oral vitamin E supplementation on the lipid profile in diabetic patients. Employing advanced search techniques on databases like PubMed, Cochrane Library, and Google Scholar, we conducted a comprehensive literature search using MeSH terms, advanced search methods, and specific eligibility criteria. The results yielded one systematic review with a meta-analysis and two randomized controlled trials (RCTs) that met the predefined PICO and eligibility criteria.
 Results: The systematic review and meta-analysis, along with one RCT, reported no significant reduction in lipid profiles with oral vitamin E supplementation in diabetic patients. In contrast, the other RCT observed an improvement in lipid profiles among diabetic patients receiving oral vitamin E supplementation.
 Conclusion: Supplementing with oral vitamin E does not enhance the lipid profile of individuals with diabetes mellitus.

Importance of Dyslipidaemia Treatment in Individuals with Type 2 Diabetes Mellitus—A Narrative Review

Type 2 diabetes mellitus (T2DM) is a common metabolic disease characterised by insulin resistance and elevated blood glucose levels, affecting millions of people worldwide. T2DM individuals with dyslipidaemia have an increased risk of cardiovascular disease (CVD). A complex interplay of risk factors such as hyperglycaemia, dyslipidaemia, hypertension, obesity, inflammation, and oxidative stress favour the development of atherosclerosis, a central mechanism in the pathogenesis of cardiovascular disease. Dyslipidaemia, a hallmark of T2DM, is characterised by elevated triglycerides, decreased high-density lipoprotein (HDL) cholesterol and the presence of small, dense low-density lipoprotein (LDL) particles, all of which promote atherosclerosis. In this article, we have attempted to present various treatment strategies that include pharmacological interventions such as statins, ezetimibe, PCSK9 inhibitors, fibrates, and omega-3 fatty acids. We have also tried to highlight the pivotal role of lifestyle modifications, including physical activity and dietary changes, in improving lipid profiles and overall cardiovascular health in T2DM individuals. We have also tried to present the latest clinical guidelines for the management of dyslipidaemia in T2DM individuals. In conclusion, the treatment of dyslipidaemia in T2DM individuals is of great importance as it lowers lipid particle levels, slows the progression of atherosclerosis, and ultimately reduces susceptibility to cardiovascular disease.

Abstract 17147: Hypertriglyceridemia Associated With Peritoneal Dialysis

Introduction: Chronic kidney disease and kidney replacement therapies (KRT) are associated with increased incidence of dyslipidemia and cardiovascular disease. In patients with chronic kidney disease, uremic dyslipidemia can cause qualitative and quantitative changes in the lipoproteins due to inflammation, malnutrition, and proteinuria. The major abnormalities include increase in triglyceride (TG) rich particles and reduced activity of lipoprotein lipase (LP). In this case, we present a patient who developed worsening hypertriglyceridemia after KRT changed to peritoneal dialysis (PD). Clinical Course: A 65-year-old female with end stage renal disease (ESRD) on PD, mixed dyslipidemia and hypertension who presented for elevated triglycerides 2084 mg/dL. Patient had been on KRT for 5 years and was switched to PD for the past 3 years. TG prior to starting PD was 203 mg/dL. Patient was started on atorvastatin 40 mg daily, Omega-3 Fatty Acids 2 g twice daily and substituted hypertonic glucose exchange with icodextrin for dialysate. TG improved to 391 mg/dL with these changes. Discussion: Hypertriglyceridemia is a common condition with management include lifestyle modifications and medications. In uremic dyslipidemia, there is increase in triglyceride-rich lipoproteins, small dense low-density lipoprotein particles, increased lipoprotein (a), and decreased high density lipoprotein. The pathogenesis of hypertriglyceridemia seen in PD is not well understood. There is overproduction of very low-density lipoprotein, peritoneal protein loss through drained dialysate, carbohydrate loading from the glucose based dialysate and reduced LP function contributing to the hypertriglyceridemia. This patient’s TG worsened when she was switched to PD from hemodialysis. TG improved with lifestyle modifications, medications and change in dialysate fluids. Hypertriglyceridemia associated with PD is rare, but it is important to recognize and treat to reduce risk of pancreatitis and cardiovascular complications.

The Importance of Metabolic and Environmental Factors in the Occurrence of Oxidative Stress during Pregnancy.

Metabolic changes in pregnant women begin in the first weeks after conception under the influence of placental hormones that affect the metabolism of all nutrients. An increased concentration of total lipids accompanies pregnancy and an increased accumulation of triglycerides in low-density lipoproteins (LDL) particles. Lipids in small dense LDL particles are more susceptible to oxidative modification than normal-density LDL particles. Unlike LDL high-density lipoproteins (HDL), lipoprotein particles have an atheroprotective role in lipid metabolism. The very growth of the fetus depends on the nutrition of both parents, so obesity is not only in the mother but also in the father. Nutritional programming of the offspring occurs through changes in lipid metabolism and leads to an increased risk for cardiometabolic diseases. Pregnancy is accompanied by an increased need for oxygen in the mitochondria of the placenta and a tendency to develop oxidative stress. Oxidative stress represents a disturbance in the balance of oxidation-reduction processes in the body that occurs due to the excessive production of free oxygen radicals that cellular homeostatic mechanisms are unable to neutralize. When the balance with the antioxidant system is disturbed, which happens when free oxygen radicals are in high concentrations, serious damage to biological molecules occurs, resulting in a series of pathophysiological and pathological changes, including cell death. Therefore, oxidative stress plays a significant role in the pathogenesis of many complications that can occur during pregnancy. The oxidative status of pregnant women is also influenced by socioeconomic living conditions, lifestyle habits, diet, smoking, and exposure to environmental air pollution. During a healthy pregnancy, the altered lipid profile and oxidative stress create an increased risk for premature birth and pregnancy-related diseases, and a predisposition to adult diseases.

Effect of Semaglutide on Subclinical Atherosclerosis and Cardiometabolic Compensation: A Real-World Study in Patients with Type 2 Diabetes.

Semaglutide is a recently approved glucagon-like peptide-1 receptor agonist. Several trials reported the protective effect of injectable semaglutide on cardiovascular (CV) risk by reducing major adverse cardiovascular events in type 2 diabetes patients. Strong preclinical evidence supports the CV benefits of semaglutide through an effect on atherosclerosis. However, scant evidence is available about the protective mechanisms of semaglutide in clinical practice. A retrospective observational study was conducted among consecutive type 2 diabetes patients treated with injectable semaglutide in Italy between November 2019 and January 2021 when the drug was first available in the country. The primary aims were the assessment of the carotid intima-media thickness (cIMT) and hemoglobin A1c (HbA1c) levels. The secondary aims were the evaluation of anthropometric, glycemic, and hepatic parameters and plasma lipids, including the assessment of the triglyceride/high-density lipoprotein ratio as an indirect marker of atherogenic small, dense low-density lipoprotein particles. Injectable semaglutide reduced HbA1c and cIMT. An improvement in CV risk factors and the triglyceride/high-density lipoprotein ratio was reported. Moreover, through correlation analyses, we found that hepatic fibrosis and steatosis indices and the anthropometric, hepatic, and glycemic parameters, as well as plasma lipids, were unrelated to the variations in cIMT and HbA1c. Our findings suggest the effect of injectable semaglutide on atherosclerosis as a key CV protective mechanism. Considering the favorable effects on atherogenic lipoproteins and hepatic steatosis indices, our results support the pleiotropic effect of semaglutide beyond glycemic control.

The Role of Advanced Glycation End Products on Dyslipidemia.

Disorders of lipoprotein metabolism and glucose homeostasis are common consequences of insulin resistance and usually co-segregate in patients with metabolic syndrome and type 2 diabetes mellitus (DM). Insulin-resistant subjects are characterized by atherogenic dyslipidemia, a specific lipid pattern which includes hypertriglyceridemia, reduced high-density lipoprotein cholesterol level, and increased proportion of small, dense low-density lipoprotein (LDL). Chronic hyperglycemia favors the processes of non-enzymatic glycation, leading to the increased production of advanced glycation end products (AGEs). Apart from direct harmful effects, AGEs are also potent inducers of oxidative stress and inflammation. In addition, increased AGEs' production may induce further qualitative modifications of small, dense LDL particles, converting them to glycated LDLs. These particles are even more atherogenic and may confer an increased cardiovascular risk. In this narrative review, we summarize the available evidence of the pathophysiological role and clinical importance of circulating AGEs and glycated LDLs in patients with dyslipidemia, particularly those with DM and related complications. In addition, we discuss recent advances and the issues that should be improved regarding laboratory assessment of AGEs and glycated LDLs, as well as the possibilities for their therapeutic modulation.

Low-density lipoprotein particles in atherosclerosis.

Among the diseases causing human death, cardiovascular disease (CVD) remains number one according to the World Health Organization report in 2021. It is known that atherosclerosis is the pathological basis of CVD. Low-density lipoprotein (LDL) plays a pivotal role in the initiation and progression of atherosclerotic CVD (ASCVD). LDL cholesterol (LDL-C) is the traditional biological marker of LDL. However, large numbers of patients who have achieved the recommended LDL-C goals still have ASCVD risk. In multiple prospective studies, LDL particle (LDL-P) is reported to be more accurate in predicting CVD risk than LDL-C. LDL-Ps differ in size, density and chemical composition. Numerous clinical studies have proved that the atherogenic mechanisms of LDL-Ps are determined not only by LDL number and size but also by LDL modifications. Of note, small dense LDL (sdLDL) particles possess stronger atherogenic ability compared with large and intermediate LDL subfractions. Besides, oxidized LDL (ox-LDL) is another risk factor in atherosclerosis. Among the traditional lipid-lowering drugs, statins induce dramatic reductions in LDL-C and LDL-P to a lesser extend. Recently, proprotein convertase subtilsin/kexin type 9 inhibitors (PCSK9i) have been demonstrated to be effective in lowering the levels of LDL-C, LDL-P, as well as CVD events. In this article, we will make a short review of LDL metabolism, discuss the discordance between LDL-C and LDL-P, outline the atherogenic mechanisms of action of LDL by focusing on sdLDL and ox-LDL, summarize the methods used for measurement of LDL subclasses, and conclude the advances in LDL-lowering therapies using statins and PCSK9i.

Clinical Utility of Small, Dense LDL as an Atherogenic Risk Marker

Low-density lipoprotein (LDL) has a major role in the origination and development of atherosclerosis and Cardio Vascular Diseases (CVD). Over the past few years, many studies have been concerned with different subclasses of LDLs and their atherogenicity. Low-density lipoproteins (LDLs) include many subclasses. The most common are large buoyant (LB), intermediate and small dense (sd) low-density lipoprotein particles. Small dense low-density lipoproteins attracted a lot of attention. Small dense LDL (sdLDL) has recently been proven to be more atherogenic than other lipoproteins containing apolipoprotein B, which have the potential to trigger atherosclerotic reactions. Many researchers have reported that small dense low-density lipoproteins are the superior biomarker for the prediction of atherosclerosis and CVDs regarding all other markers, including total low-density lipoprotein cholesterol(LDL-C), and total serum cholesterol, non-high-density lipoprotein (non-HDL-C), high-density lipoprotein cholesterol (HDL-C), and triglyceride content. Circulating small dense, low-density lipoproteins go through several modifications in the blood, rendering them more atherogenic. These modifications may include glycation, oxidation, and desialylation. Modified particles are strong inducers of inflammation resulting in many cardiovascular diseases, making them the primary target during the treatment of coronary artery disease. This article will elaborate on the clinical utility of sdLDL as an early marker to predict atherosclerosis and CVDs, and why it is considered superior to other atherosclerotic markers.

Lipid Variability and Diabetes Mellitus

Diabetic dyslipidemia is characterized by hypertriglyceridemia, low HDL (high-density lipoprotein)-cholesterol, elevated LDL (low-density lipoprotein)-cholesterol, and predominance of small dense LDL particles caused by insulin resistance in type 2 diabetes or insulin deficiency in type 1 diabetes. Dyslipidemia is a major risk factor for atherosclerotic cardiovascular disease in diabetes, and lowering lipid levels can reduce its morbidity and mortality. Current guidelines for dyslipidemia management recommend that the LDL-C goal be lower than 55~100 mg/dL depending on the underlying risk factors. However, higher visit-to-visit variability in cholesterol levels might be an independent predictor of major adverse cardiovascular events and poor renal outcomes in diabetes. In this review, we focused on clinical implications of lipid variability in diabetes.

Small dense low-density lipoprotein particles: clinically relevant?

Levels of small, dense low-density lipoprotein (LDL) (sdLDL) particles determined by several analytic procedures have been associated with risk of atherosclerotic cardiovascular disease (ASCVD). This review focuses on the clinical significance of sdLDL measurement. Results of multiple prospective studies have supported earlier evidence that higher levels of sdLDL are significantly associated with greater ASCVD risk, in many cases independent of other lipid and ASCVD risk factors as well as levels of larger LDL particles. A number of properties of sdLDL vs. larger LDL, including reduced LDL receptor affinity and prolonged plasma residence time as well as greater oxidative susceptibility and affinity for arterial proteoglycans, are consistent with their heightened atherogenic potential. Nevertheless, determination of the extent to which sdLDL can preferentially impact ASCVD risk compared with other apoprotein B-containing lipoproteins has been confounded by their metabolic interrelationships and statistical collinearity, as well as differences in analytic procedures and definitions of sdLDL. A growing body of data points to sdLDL concentration as a significant determinant of ASCVD risk. Although future studies should be aimed at determining the clinical benefit of reducing sdLDL levels, there is sufficient evidence to warrant consideration of sdLDL measurement in assessing and managing risk of cardiovascular disease. https://www.dropbox.com/s/lioohr2ead7yx2p/zoom_0.mp4?dl=0.

Atherosclerosis Development and Progression: The Role of Atherogenic Small, Dense LDL

Atherosclerosis is responsible for large cardiovascular mortality in many countries globally. It has been shown over the last decades that the reduction of atherosclerotic progression is a critical factor for preventing future cardiovascular events. Low-density lipoproteins (LDL) have been successfully targeted, and their reduction is one of the key preventing measures in patients with atherosclerotic disease. LDL particles are pivotal for the formation and progression of atherosclerotic plaques; yet, they are quite heterogeneous, and smaller, denser LDL species are the most atherogenic. These particles have greater arterial entry and retention, higher susceptibility to oxidation, as well as reduced affinity for the LDL receptor. Increased proportion of small, dense LDL particles is an integral part of the atherogenic lipoprotein phenotype, the most common form of dyslipidemia associated with insulin resistance. Recent data suggest that both genetic and epigenetic factors might induce expression of this specific lipid pattern. In addition, a typical finding of increased small, dense LDL particles was confirmed in different categories of patients with elevated cardiovascular risk. Small, dense LDL is an independent risk factor for cardiovascular diseases, which emphasizes the clinical importance of both the quality and the quantity of LDL. An effective management of atherosclerotic disease should take into account the presence of small, dense LDL in order to prevent cardiovascular complications.

Atherogenic lipidomics profile in healthy individuals with low cardiorespiratory fitness: The HUNT3 fitness study

Background and aimsLow cardiorespiratory fitness is a strong and independent risk factor for cardiovascular disease (CVD). Serum profiling of healthy individuals with large differences in cardiorespiratory fitness may therefore reveal early biomarkers of CVD development. Thus, we aimed to identify circulating lipoprotein subfractions differentially expressed between groups of individuals with large differences in cardiorespiratory fitness, measured as maximal oxygen uptake (VO2max). MethodsHealthy subjects (40–59 years) were selected from the third wave of the Trøndelag health study (HUNT3) based on having an age-dependent high VO2max (47.1 ± 7.7 mL kg−1·min−1, n = 103) or low VO2max (31.4 ± 4.9 mL kg−1·min−1, n = 108). The individuals were matched on gender, age, physical activity level and fasting status. Results99 lipoprotein subfractions were quantified in serum samples using nuclear magnetic resonance (NMR) lipidomics. Standard clinical analyses showed similar levels of total cholesterol, low-density lipoprotein (LDL)-cholesterol and high-density lipoprotein (HDL)-cholesterol between the groups, and slightly higher levels of triglycerides in participants with low VO2max. Thirteen lipoprotein subfractions were increased in the low VO2max group compared to the high VO2max group (p < 0.005), including mainly large very low-density lipoprotein (VLDL) subfractions. In addition, triglyceride levels in small-sized HDL and LDL particles were increased in participants with low VO2max. Correlation analyses between VO2max and lipoproteins subfractions displayed a negative correlation between VO2max and the levels of cholesterol and phospholipids in the small HDL particles. The lipoprotein profile of individuals with low VO2max is similar to the profile of insulin resistant individuals. ConclusionsLow VO2max was associated with enrichment of large VLDL particles, as well as an increased triglycerides content in the small and dense HDL and LDL particles. This unfavorable lipid profile is likely to be involved in the strong associations between VO2max and CVD.

Obesity Pillars Roundtable: Obesity and South Asians

BackgroundCompared to other races/ethnicities, individuals from South Asia with obesity are strikingly susceptible to the presence of CVD risk factors and onset of CVD events – in part due to adiposopathic anatomic and metabolic responses to positive caloric balance. Pathogenic endocrine and immune effects of adipocyte hypertrophy and visceral fat accumulation both directly and indirectly promote among the most common metabolic diseases encountered in clinical practice – many being major cardiovascular disease (CVD) risk factors. This is especially applicable to those from South Asia – largely due to genetics, epigenetics, unhealthful nutrition, and physical inactivity. MethodsThis roundtable discussion included 4 obesity specialists engaged in the clinical management of obesity among patients of South Asian descent. ResultsPatients with obesity from South Asia have increased adipocyte size, fewer (functional) adipocytes, and increased visceral adiposity accompanied by functional endocrine and immune abnormalities. This helps explain the increased CVD risk factors and increased CVD risk among this unique population. These CVD risk factors include increased prevalence of metabolic syndrome (even at lower body mass index relative to other races), insulin resistance, type 2 diabetes mellitus, increased lipoprotein (a), and adiposopathic dyslipidemia [(i.e., elevated triglyceride levels, reduced high density lipoprotein cholesterol levels, increased low density lipoprotein (LDL) particle number, and increased prevalence of smaller and denser LDL particles]. ConclusionThe four panelists of this roundtable discussion describe their practical diagnostic processes and treatment plans for patients from South Asia, with an emphasis on a patient-centered approach to obesity in this unique population.

Uticaj metaboličkih parametara na veličinu i subklasu LDL i HDL kod adolescenata sa dijabetesom tip 1

Alterations in the serum of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) size and subclass contribute to the atherogenesis in coronary artery disease in diabetic patients. The purpose of this study is to evaluate the effect of metabolic parameters on LDL and HDL size and subclasses in adolescents with type 1 diabetes. The cross-sectional study included 43 adolescents (23 females, 20 males) with type 1 diabetes of mean age 15.09±1.94 years, with mean disease duration of 5.86 ± 3.08 years. LDL and HDL particles were separated by polyacrylamide gradient gel electrophoresis, while serum lipid parameters were determined by routine laboratory methods. Patients with inadequate metabolic control (HbA1c ≥ 7.5%) had a higher mean value of triglycerides (TG) (p = 0.041), higher proportions of small, dense LDL particles (p = 0.045), higher proportions of LDL IIA subclasses (p=0.03) and smaller LDL diameter (p = 0.02) and HDL diameter (p = 0.04) than patients with optimal metabolic control (HbA1c &lt; 7.5%). Higher HbA1c and higher TG levels were statistically significantly related to small, dense LDL (r=0.341, p=0.025; r= 0.394, p= 0.009) and HDL particles (r=0.684, p=0.000; r=0.421, p=0.005). Predictors of small, dense LDL and HDL particles, which contribute to atherogenesis, were high HbA1c (HR = 1.52, 95% CI: 0.97-2.40; HR 3.87, 95% CI: 2.11-7.10) and elevated TG (HR= 1.10, 95% CI: 1.00-1.20; HR 1.85, 95% CI: 1.07-3.21). Diabetic adolescents require particular attention in order to minimize factors such as high HbA1c and elevated TGs in the development of future cardiovascular events.

Biomarkeri dislipidemije kod pacijenata sa dijabetesnim stopalom

Diabetic foot (DF) is one of the most severe complications of diabetes that significantly reduces the quality of life and survival of patients. Besides firmly established risk factors, novel data indicate that alterations in lipid metabolism might also be implicated in the development and progression of DF. Diabetic dyslipidemia is characterized by the atherogenic triad, consisting of increased triglycerides (TG), decreased high-density lipoprotein cholesterol (HDL-C) levels and the presence of small, dense low-density lipoprotein (LDL) particles. Accumulating evidence suggests that profound hypertriglyceridemia and HDL-C reduction are common findings in patients with diabetic neuropathy and significantly contribute to an increased risk for DF, amputation and mortality. Small, dense LDL particles play an important role in the development of cardiovascular complications of diabetes, but their clinical importance in patients with DF remains to be established. In this paper, we will discuss the significance of standard and novel lipid biomarker determination in the assessment of the risk for the development and progression of DF.

Diabetes and Colorectal Cancer Risk: A New Look at Molecular Mechanisms and Potential Role of Novel Antidiabetic Agents.

Epidemiological data have demonstrated a significant association between the presence of type 2 diabetes mellitus (T2DM) and the development of colorectal cancer (CRC). Chronic hyperglycemia, insulin resistance, oxidative stress, and inflammation, the processes inherent to T2DM, also play active roles in the onset and progression of CRC. Recently, small dense low-density lipoprotein (LDL) particles, a typical characteristic of diabetic dyslipidemia, emerged as another possible underlying link between T2DM and CRC. Growing evidence suggests that antidiabetic medications may have beneficial effects in CRC prevention. According to findings from a limited number of preclinical and clinical studies, glucagon-like peptide-1 receptor agonists (GLP-1RAs) could be a promising strategy in reducing the incidence of CRC in patients with diabetes. However, available findings are inconclusive, and further studies are required. In this review, novel evidence on molecular mechanisms linking T2DM with CRC development, progression, and survival will be discussed. In addition, the potential role of GLP-1RAs therapies in CRC prevention will also be evaluated.

Association of serum 25-Hydroxy Vitamin D level with lipid, lipoprotein, and apolipoprotein level

ABSTRACT Introduction 25-Hydroxy vitamin D (Vit D3) deficiency was found to be associated with vascular dysfunction, arterial stiffening, extent of coronary artery disease and cardiovascular mortality. Previous studies showed positive correlation between serum Vit D3 and HDL-C and negative correlation between Vit D3 and LDL-C. The aim of this study is to investigate more details about the possible association of serum Vit D3 level with lipid, lipoprotein and apolipoprotein level. Methods Totally 101 patients were included in this study and Vit D3, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), High-density lipoprotein cholesterol (HDL-C), total triglyceride (TG), non-high-density lipoprotein cholesterol (Non-HDL-C), low-density lipoprotein particle (LDL-P), small dense low-density lipoprotein particle (sLDL-P), small dense low-density lipoprotein cholesterol (sdLDL-C), High-density lipoprotein cholesterol particles (HDL-P), High-density lipoprotein 2-cholesterol (HDL2-C), Apolipoprotein B(ApoB), Apolipoprotein A1 (Apo A1) and Apolipoprotein B/Apolipoprotein A1 ratio (ApoB/A ratio) were tested. Results Our results show that patients with Vit D3 deficiency (Vit D3 < 30 ng/ml) have significantly higher level of LDL-C, TG, Non-HDL-C, LDL-P, sLDL-P, sdLDL-C, ApoB and ApoB/A ratio compare with patients have normal Vit D3 level (Vit D3 > 30 ng/ml). Patients with normal Vit D3 level have significantly higher level of HDL-C and HDL2-C. Correlation study shows that Vit D3 level is negative correlated with TC, LDL-C, TG, Non-HDL-C, LDL-P, sLDL-P, sdLDL-C, ApoB and ApoB/A ratio and positive correlated with HDL2-C level. Conclusion Our results show that Vit D3 deficiency links to an increased risk for dyslipidemia and that may be the reason that patients with vitamin D deficiency tend to have higher risk of coronary artery disease.

Mitochondrial Lipid Homeostasis at the Crossroads of Liver and Heart Diseases.

The prevalence of NAFLD (non-alcoholic fatty liver disease) is a rapidly increasing problem, affecting a huge population around the globe. However, CVDs (cardiovascular diseases) are the most common cause of mortality in NAFLD patients. Atherogenic dyslipidemia, characterized by plasma hypertriglyceridemia, increased small dense LDL (low-density lipoprotein) particles, and decreased HDL-C (high-density lipoprotein cholesterol) levels, is often observed in NAFLD patients. In this review, we summarize recent genetic evidence, proving the diverse nature of metabolic pathways involved in NAFLD pathogenesis. Analysis of available genetic data suggests that the altered operation of fatty-acid β-oxidation in liver mitochondria is the key process, connecting NAFLD-mediated dyslipidemia and elevated CVD risk. In addition, we discuss several NAFLD-associated genes with documented anti-atherosclerotic or cardioprotective effects, and current pharmaceutical strategies focused on both NAFLD treatment and reduction of CVD risk.

Inverse association between serum endocan levels and small LDL and HDL particles in patients with type 2 diabetes mellitus.

Determination of lipoprotein size and subclasses distribution can provide more significant information on cardiovascular disease risk than measurement of traditional lipid parameters alone. Accordingly, we aimed to examine their potential relationship with the novel biomarker of endothelial dysfunction, such as endocan in patients with type 2 diabetes mellitus (T2D), since there are no studies concerning this issue. This case-control study included a total of 42 individuals with T2D and 64 diabetes-free participants. Serum endocan, lipid parameters, and lipoprotein subclasses were measured. Patients with T2D exhibited higher proportion of the smallest high-density lipoprotein (HDL) particles HDL 3c, as compared with diabetes-free participants (p=0.047). Higher serum endocan levels in T2D patients with low small dense low-density lipoprotein (LDL) particles (sdLDL) %, as compared with corresponding group of diabetes-free subjects was shown (p<0.01). Univariate binary logistic analysis revealed significant positive association of endocan and LDL diameter (OR=1.686, p=0.004), and negative associations of endocan with proportions of sdLDL (OR=0.928, p=0.007) and HDL3b (OR=0.789, p=0.009) particles. In a multivariate analysis, LDL diameter and proportions of sdLDL and HDL3b subclasses remained independent predictors of endocan levels in tested population. The results of our study showed that larger LDL diameters, but lower sdLDL and HDL3b proportions were associated with higher endocan levels in population with T2D. More studies in the future are needed to confirm the observed relationship and to examine its causal nature.

Dietary Patterns and Health Outcomes among African American Maintenance Hemodialysis Patients.

The association between dietary patterns and health outcomes, such as quality of life (QOL), in maintenance hemodialysis (MHD) patients with certain racial backgrounds has not been studied in detail. QOL is a powerful outcome measure in which dietary patterns could be a modifying factor. This study is a secondary analysis examining the association between dietary patterns and health outcomes in 101 African American (AA) maintenance hemodialysis (MHD) patients participating in the Palm Tocotrienols in Chronic Hemodialysis (PATCH) study. Quality of life (QOL) was assessed using the Kidney Disease Quality of Life 36-item survey (KDQOL-36™). Blood samples were analyzed for lipids, lipoprotein subfractions, and inflammatory markers. Food intake was measured using six non-consecutive 24-h dietary recalls over 15 months. Implausible energy intake reports were screened out by comparing reported energy intake (rEI) with predicted total energy expenditure (pTEE). Cluster analysis, using the k-means algorithm, identified two distinct dietary patterns in the study population: a high “sugar sweetened beverage” pattern (hiSSB) and a low “sugar sweetened beverage pattern” (loSSB). In the hiSSB group, consumption of SSB accounted for ~28% of energy intake, while SSB represented only 9% of energy intake in the loSSB group. The hiSSB group was characterized by a higher intake of total calories, sugar and percentage of kilocalories from carbohydrates, whereas the percentage of kilocalories from protein and fat was lower. While additional micronutrient intakes differed between groups (vitamin C, zinc, chromium), these were significantly lower than recommended values in the entire cohort. Patients in the hiSSB group presented with lower high-density lipoprotein cholesterol (HDL-C), lower large HDL particles and smaller low density lipoprotein (LDL) particle diameters. Antidepressant usage was significantly higher in the hiSSB group. Patients in the hiSSB group scored lower across all five KDQOL domains and scored significantly lower in the mental composite domain. MHD patients following a hiSSB dietary pattern had smaller dense LDL particles, lower HDL-C, and a lower QOL. Suboptimal intakes of fruits, vegetables, and grains as well as key micronutrients were evident in both patterns.