Levels Of Apolipoprotein Research Articles

Neurodegeneration Markers Galectin-3 and Apolipoprotein E Are Elevated in the Aqueous Humor of Eyes With Glaucoma.

Galectin-3 (Gal-3) and apolipoprotein E (APOE) are markers of activated microglia in neurodegenerative diseases of the central nervous system, whose targeting is protective in mouse models of glaucoma. In this study, we examined levels of Gal-3 and APOE in human aqueous humor (AH) and defined their clinical associations with glaucoma. We collected AH from 59 glaucoma patients and 15 controls at the start of planned ophthalmic surgery. Gal-3 and APOE levels were quantified by enzyme-linked immunosorbent assay. Total protein in AH was quantified by bicinchoninic acid assay. Significant associations between Gal-3, APOE, and clinical covariates were defined using univariate and multivariate linear regression models. Gal-3 and APOE levels were significantly elevated in the AH of glaucoma patients compared to controls (P = 0.004 and P < 0.001, respectively). Gal-3 and APOE were positively correlated across the entire cohort (r = 0.65, P = 6.2E-9). No association was observed between Gal-3 and total protein or APOE and total protein (P = 0.35 and P = 0.50, respectively), indicating that their levels were not increased in glaucomatous AH due to nonspecific protein accumulation. Multivariate linear regression modeling revealed significant associations between Gal-3 and maximum recorded intraocular pressure (P = 0.009) and between APOE and number of past ophthalmic surgeries (P = 0.031). We demonstrate that Gal-3 and APOE are significantly elevated in the AH of eyes with glaucoma and are associated with a history of poorly controlled disease. Gal-3 and APOE in AH may inform clinical decision-making as quantifiable readouts of microglial activation in eyes with glaucoma.

Apolipoprotein B level in corona virus patients in Iraq

Background: Since the outbreak of the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in December 2019, it has affected &gt;200 countries, areas, or territories in 6 continents. At present, whether COVID-19 has an effect on thyroid function is unclear. The aim of this study was to evaluate Apolipoprotein in iraqi patients with COVID-19. Methods: Clinical features, laboratory results, and real time PCR were reviewed for 60 patients with laboratory-confirmed COVID-19. They were admitted to the Al-Sadr Teaching Hospital; Iraq between September and December 2021. Healthy participants who underwent routine physical checkups and non-COVID-19 patients the study as the control group. Apolipoprotein B and Fibrinogen levels were determine and compared between the COVID-19 and control groups. Results: Fibrinogen protein B lower than the normal range of the patients with COVID-19 Compared to the control group. The levels of Apolipoprotein of the patients with COVID-19 were significantly lower than those of the healthy control group. The lower the Fg and ABOB levels were, with statistical significance (p &lt;0.001). Conclusions The Changing fibrinogen and apolipoprotein B in the blood of people with Coronavirus may have a role in the infection and the life cycle of the virus.

Cholesterol Content of Very-Low-Density Lipoproteins Is Associated with 1-Year Mortality in Acute Heart Failure Patients.

Considering the relationship between the extent of metabolic derangement and the disease severity in heart failure, we hypothesized that the lipid content of very-low-density lipoprotein (VLDL) may have prognostic value for 1 year mortality in acute heart failure (AHF). Baseline serum levels of VLDL cholesterol (VLDL-C), VLDL triglycerides (VLDL-TG), VLDL phospholipids (VLDL-PL), and VLDL apolipoprotein B (VLDL-apoB) were measured using NMR spectroscopy. We calculated the ratios of the respective VLDL lipids and VLDL apoB (VLDL-C/VLDL-apoB, VLDL-TG/VLDL-apoB, and VLDL-PL/VLDL-apoB), as estimators of the cholesterol, triglyceride, and phospholipid content of VLDL particles and tested their association with mortality. Out of 315 AHF patients, 118 (37.5%) patients died within 1 year after hospitalization for AHF. Univariable Cox regression analyses revealed a significant inverse association of VLDL-C/VLDL-apoB (hazard ratio (HR) 0.43, 95% confidence interval (CI) 0.29–0.64, p < 0.001), VLDL-TG/VLDL-apoB (HR 0.79, 95% CI 0.71–0.88, p < 0.001), and VLDL-PL/VLDL-apoB (HR 0.37, 95% CI 0.25–0.56, p < 0.001) with 1 year mortality. Of the tested parameters, only VLDL-C/VLDL-apoB remained significant after adjustment for age and sex, as well as other clinical and laboratory parameters that showed a significant association with 1 year mortality in the univariable analyses. We conclude that cholesterol content of circulating VLDL (VLDL-C/VLDL-apoB) might be of prognostic value in AHF.

Discordance of apolipoprotein B with low-density lipoprotein cholesterol or non-high-density lipoprotein cholesterol and coronary atherosclerosis.

High level of apolipoprotein B (Apo B) is associated with incident subclinical atherosclerosis. The present study evaluated the associations between discordant Apo B with low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), and coronary atherosclerotic burden. This study enrolled 3043 participants aged 50-75 years from the PolyvasculaR Evaluation for Cognitive Impairment and vaScular Events (PRECISE) study that was conducted in the community in Lishui City, China. Discordant Apo B with LDL-C and non-HDL-C were defined by residuals and medians. Coronary atherosclerotic burden was evaluated by segment involvement score (SIS) and segment stenosis score (SSS) which were determined by computed tomography angiography. We performed discordance analyses examining associations of discordant Apo B with LDL-C or non-HDL-C with the coronary atherosclerotic burden. The mean age of participants was 61.2 ± 6.7 years, 53.6% were females. Participants with discordant high Apo B relative to non-HDL-C were at higher odds of plaques [odds ratio (OR), 1.30; 95% confidence interval (CI), 1.08-1.57], SIS [common odds ratio (cOR), 1.35; 95% CI, 1.14-1.60], and SSS (cOR, 1.40; 95% CI, 1.18-1.67) compared with concordant group. However, discordantly low Apo B with non-HDL-C was associated with decreased odds of the coronary atherosclerotic plaques and its burden. Similar results were shown for discordant analyses for Apo B with LDL-C. Discordantly high Apo B with LDL-C and non-HDL-C were associated with an increased odds of the coronary atherosclerotic plaques and its burden. These findings highlighted the importance of Apo B for primary prevention of coronary atherosclerosis.

Associations between maternal mid-pregnancy apolipoprotein A-1, apolipoprotein B, apolipoprotein B/apolipoprotein A-1 ratio and preterm birth

Background and aimsElevated lipid levels during pregnancy have been shown to be related to the risk of preterm birth. Despite the importance of apolipoprotein (Apo) in lipid metabolism and transportation, evidence regarding apolipoprotein levels during pregnancy and preterm birth is still limited. Therefore, we aim to investigate the associations between maternal ApoA-1, ApoB, ApoB/ApoA-1 ratio and preterm birth. Materials and methData were extracted from the information system of Guangdong Women and Children Hospital. Lipoprotein levels were tested using Beckman Coulter AU5800 in mid-pregnancy at a median gestational age of 18 w. Maternal serum ApoB, ApoA-1 and ApoB/ApoA-1 ratio were categorized into tertiles. Logistic regression models were performed to evaluate the odds ratios and 95% confidence intervals for preterm birth. ResultsA total of 5,986 maternal-newborn pairs were included in this study. The rate of preterm birth was 5.7% (n = 344). The multivariate-adjusted ORs (95% CI) of preterm birth were 1.51 (1.06, 2.10) for individuals with high ApoB (>90th), 0.63 (0.38, 0.99) for those with low ApoB (<10th), and 1.64 (1.18, 2.24) for those with high ApoB/ApoA-1 (>90th). Subgroup analyses showed that the association of ApoB and preterm birth was only significant among women with pre-pregnancy BMI 18.5-24 kg/m2 (OR = 1.36, 95% CI: 1.12–1.65), age at delivery ≥ 35 years (OR = 1.43, 95% CI: 1.12–1.83). ConclusionElevated maternal ApoB level and ApoB/ApoA-1 ratio during mid-pregnancy were related to increased risk of preterm birth. Monitoring maternal serum apolipoprotein levels may help to identify the high-risk population of preterm birth.

Apolipoproteins-New Biomarkers of Overweight and Obesity among Childhood Acute Lymphoblastic Leukemia Survivors?

Patients suffering from childhood acute lymphoblastic leukemia (ALL) are at risk of late adverse treatment-related effects. The examination of targeted biomarkers could be used to improve the diagnosis and prediction of life-threatening ALL sequelae. The purpose of this cross-sectional study was to search for treatment-related alterations in apolipoprotein (Apo) levels as potential markers of the occurrence of obesity in subjects treated for ALL, and to assess the relationships between weight, gender, anticancer treatment, and Apo concentrations. Fifty-eight ALL survivors were included in the study. The mean time of follow-up after treatment cessation was 5.41 ± 4.29 years. Serum levels of apolipoproteins were measured using a multiplex assay kit. Among ALL survivors, we observed a significant correlation of Apo-C1, Apo-C3, Apo-H, and Apo-J levels, depending on body mass index (BMI). Marked differences were observed in the area under the curve of Apo-A1, Apo-A2, Apo-C1, Apo-D. In our study, patients with a history of childhood ALL developed alterations in their Apo profile. Furthermore, this is the first study revealing that some apolipoproteins may act as valuable biomarkers useful in the prognosis of metabolic imbalance. We believe that this paper, at least partially, will highlight the importance of long-term prognosis of metabolic complications associated with the anticancer chemotherapy used to treat hematological malignancies in children.

The effect of short post-apnea time on plasma triglycerides, lipoprotein and cholesterol derived oxysterols levels

Abstract Objectives Apnea diving is characterized by extreme hypoxia and hypercapnia. Possible pathophysiological processes concerning the cardiovascular system are not yet fully understood. Hypoxia has effects on triglyceride metabolism and circulating blood lipids. To date, in voluntary apnea divers, no short-time hypoxia expositions focusing on plasma triglycerides, lipoprotein and cholesterol derived oxysterols levels have been performed. We hypothesize that short time hypoxemia leads to altered triglyceride, cholesterol, and oxysterol plasma levels in voluntary apnea divers. Methods Ten athletes performed apnea under dry conditions in a horizontal position. Plasma levels of lipids, lipoproteins and oxysterols were determined with turbidimetric immunoassays, gas chromatography (GC) - flame ionization detection (FID) and GC-MS-SIM before apnea, immediately after apnea and 0.5 h after apnea. All sterols and oxysterols were corrected for GC-FID cholesterol as measured in the same sample. Spearman’s rank correlation test was performed and pairwise comparison of absolute and cholesterol corrected plasma levels from the different sampling dates was conducted using a robust mixed linear model. Results We observed significantly reduced levels of apolipoprotein B, triglycerides, cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, and oxysterols (7β-OHC, 24-OHC, 27-OHC and 7-KC) for different time points. Cholesterol corrected plasma levels of the oxysterols showed no significant changes after short post-apnea time except for a significant elevation of the cholestane-3β, 5α, 6β-triol ratio. Conclusions We could observe that a single short time hypoxemia under dry conditions in voluntary apnea divers leads to altered triglyceride, cholesterol and oxysterol plasma levels.

Misuse of Cardiac Lipid upon Exposure to Toxic Trace Elements-A Focused Review.

Heavy metals and metalloids like cadmium, arsenic, mercury, and lead are frequently found in the soil, water, food, and atmosphere; trace amounts can cause serious health issues to the human organism. These toxic trace elements (TTE) affect almost all the organs, mainly the heart, kidney, liver, lungs, and the nervous system, through increased free radical formation, DNA damage, lipid peroxidation, and protein sulfhydryl depletion. This work aims to advance our understanding of the mechanisms behind lipid accumulation via increased free fatty acid levels in circulation due to TTEs. The increased lipid level in the myocardium worsens the heart function. This dysregulation of the lipid metabolism leads to damage in the structure of the myocardium, inclusive fibrosis in cardiac tissue, myocyte apoptosis, and decreased contractility due to mitochondrial dysfunction. Additionally, it is discussed herein how exposure to cadmium decreases the heart rate, contractile tension, the conductivity of the atrioventricular node, and coronary flow rate. Arsenic may induce atherosclerosis by increasing platelet aggregation and reducing fibrinolysis, as exposure interferes with apolipoprotein (Apo) levels, resulting in the rise of the Apo-B/Apo-A1 ratio and an elevated risk of acute cardiovascular events. Concerning mercury and lead, these toxicants can cause hypertension, myocardial infarction, and carotid atherosclerosis, in association with the generation of free radicals and oxidative stress. This review offers a complete overview of the critical factors and biomarkers of lipid and TTE-induced cardiotoxicity useful for developing future protective interventions.

Diagnostic Potential of Autophagy-5 Protein, Apolipoprotein B-48, and Oxidative Stress Markers in Serum of Patients with Early-Stage Ischemic Stroke

Strokes are among the leading causes of death worldwide and have different characteristics. Different physiopathological mechanisms characterize the numerous subtypes of ischemic stroke (IS). In this study, we investigated the relationship between serum levels of autophagy-5 protein, apolipoprotein B-48, and oxidative stress markers in patients with ischemic stroke. For this study, 100 participants were recruited, of which 50 were patients with IS and 50 were healthy individuals. We conducted a case-control study at Imam Reza Hospital from March 2019 to April 2020. Serum levels of ATG5, apo B-48, and oxidative stress markers were determined in both groups. Our Receiver Operating Characteristic Analysis evaluated the additional diagnostic value of these factors in both groups. Diabetes, smoking, age, sex, alcohol consumption, weight, and height did not differ significantly between the 2 groups (P>0.05). However, the 2 groups had significant differences in hypertension and body mass index (P<0.05). Fifty-four percent (27 patients) of patients with IS had an ischemic stroke in large vessels, while 46% (23 patients) had an ischemic stroke in small vessels. Serum levels of ATG5, apo B-48, and oxidative stress markers were higher in the case group than in the control group (P<0.0001). In patients with IS, serum levels of ATG5, apoB-48, malonaldehyde, total oxidative stress, and total antioxidant capacity can be used as novel biomarkers to predict or treat the disease.

Plasma apolipoprotein E levels in longitudinally followed patients with mild cognitive impairment and Alzheimer’s disease

BackgroundLow levels of plasma apolipoprotein E (apoE) and presence of the APOE ε4 allele are associated with an increased risk of Alzheimer’s disease (AD). Although the increased risk of AD in APOE ε4-carriers is well-established, the protein levels have received limited attention.MethodsWe here report the total plasma apoE and apoE isoform levels at baseline from a longitudinally (24 months) followed cohort including controls (n = 39), patients with stable amnestic mild cognitive impairment during 24 months follow up (MCI-MCI, n = 30), patients with amnestic MCI (aMCI) that during follow-up were clinically diagnosed with AD with dementia (ADD) (MCI-ADD, n = 28), and patients with AD with dementia (ADD) at baseline (ADD, n = 28). We furthermore assessed associations between plasma apoE levels with cerebrospinal fluid (CSF) AD biomarkers and α-synuclein, as well as both CSF and plasma neurofilament light chain (NfL), YKL-40 and kallikrein 6.ResultsIrrespective of clinical diagnosis, the highest versus the lowest apoE levels were found in APOE ε2/ε3 versus APOE ε4/ε4 subjects, with the most prominent differences exhibited in females. Total plasma apoE levels were 32% and 21% higher in the controls versus MCI-ADD and ADD patients, respectively. Interestingly, MCI-ADD patients exhibited a 30% reduction in plasma apoE compared to MCI-MCI patients. This decrease appeared to be associated with brain amyloid-β (Aβ42) pathology regardless of disease status as assessed using the Amyloid, Tau, and Neurodegeneration (A/T/N) classification. In addition to the association between low plasma apoE and low levels of CSF Aβ42, lower apoE levels were also related to higher levels of CSF total tau (t-tau) and tau phosphorylated at Threonine 181 residue (p-tau) and NfL as well as a worse performance on the mini-mental-state-examination. In MCI-ADD patients, low levels of plasma apoE were associated with higher levels of CSF α-synuclein and kallikrein 6. No significant correlations between plasma apoE and the astrocytic inflammatory marker YKL40 were observed.ConclusionsOur results demonstrate important associations between low plasma apoE levels, Aβ pathology, and progression from aMCI to a clinical ADD diagnosis.

Prevalence and clinical characteristics of metabolically healthy obese versus metabolically unhealthy obese school children.

IntroductionChildren with obesity in the absence of traditional cardiometabolic risk factors (CRF) have been described as metabolically healthy obese (MHO). Children with MHO phenotype has a favorable metabolic profile with normal glucose metabolism, lipids, and blood pressure compared to children with metabolically unhealthy obese (MUO) phenotype. This study aimed to compare several parameters related to obesity between these two groups and to examine the predictors associated with the MHO phenotype.MethodsThis study included a cross-sectional baseline data of 193 children with obesity (BMI z-score > +2 SD) aged 8-16 years enrolled in MyBFF@school program, a school-based intervention study conducted between January and December 2014. Metabolic status was defined based on the 2018 consensus-based criteria with MHO children had no CRF (HDL-cholesterol > 1.03 mmol/L, triglycerides ≤ 1.7 mmol/L, systolic and diastolic blood pressure ≤ 90th percentile, and fasting plasma glucose ≤ 5.6 mmol/L). Those that did not meet one or more of the above criteria were classified as children with MUO phenotype.ResultsThe prevalence of MHO was 30.1% (95% CI 23.7 – 37.1) among schoolchildren with obesity and more common in younger and prepubertal children. Compared to MUO, children with MHO phenotype had significantly lower BMI, lower waist circumference, lower uric acid, higher adiponectin, and higher apolipoprotein A-1 levels (p < 0.01). Multivariate logistic regression showed that adiponectin (OR: 1.33, 95% CI 1.05 – 1.68) and apolipoprotein A-1 (OR: 1.02, 95% CI 1.01 – 1.03) were independent predictors for MHO phenotype in this population.ConclusionsMHO phenotype was more common in younger and prepubertal children with obesity. Higher serum levels of adiponectin and apolipoprotein A-1 increased the possibility of schoolchildren with obesity to be classified into MHO phenotype.

Proteomics and bioinformatics analysis of follicular fluid from patients with polycystic ovary syndrome.

Objectives: Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder with heterogeneous manifestations and complex etiology. We used quantitative proteomics analysis based on mass spectrometry to identify the differences in proteomics profiles for follicular fluid obtained from patients with or without PCOS and explore possible mechanisms underlying PCOS. Methods: Follicular fluid samples were collected from infertile patients with (n = 9) or without (n = 9) PCOS. Total protein was extracted, quantitatively labeled with a tandem mass tag (TMT), and analyzed using liquid chromatography-mass spectrometry (LC‐MS). TMT-based proteomics and bioinformatics analysis were used to determine the differentially expressed proteins (DEPs) and understand the protein networks. The analysis included protein annotation, unsupervised hierarchical clustering, functional classification, functional enrichment and clustering, and protein-protein interaction analysis. Selected DEPs were confirmed by ELISA, and correlation analysis was performed between these DEPs and the clinical characteristics. Results: In this study, we have identified 1,216 proteins, including 70 DEPs (32 upregulated proteins, 38 downregulated proteins). Bioinformatics analysis revealed that the inflammatory response, complement and coagulation cascades, activation of the immune response, lipid transport, and regulation of protein metabolic processes were co-enriched in patients with PCOS. Based on ELISA results, insulin-like growth factor binding protein 1 (IGFBP1) and apolipoprotein C2 (APOC2) were differentially expressed between patients with and without PCOS. Follicular IGFBP1 showed a positive correlation with the serum levels of high-density lipoprotein cholesterol (HDL-C) (r = 0.3046, p = 0.0419), but negatively correlated with the serum levels of anti-Müllerian hormone (AMH) (r = –0.2924, p = 0.0354) and triglycerides (r = –0.3177, p = 0.0246). Follicular APOC2 was negatively correlated with the serum apolipoprotein A1 (APOA1) levels (r = 0.4509, p = 0.0002). Conclusion: Our study identified DEPs in the follicular fluid of patients with PCOS. Inflammatory response, complement and coagulation cascades, activation of the immune response, lipid transport, and regulation of protein metabolic process were deregulated in PCOS, which may play essential roles in the pathogenesis of PCOS.

The association between serum lipid levels and histological type of breast cancer

BackgroundStudies have investigated the association between serum lipids level or apolipoprotein levels and breast cancer (BC) risk. However, the relationship between serum lipids level and apolipoprotein levels and histological type of breast cancer remains unclear. This study was aimed to explore the association between serum lipids level and the histological type of BC, particularly to estrogen receptor (ER) and progesterone receptor (PR) positive BC.Materials and methods220 cases of pathology-confirmed BC were retrospectively collected in this study. Patients’ demographic information, clinical data, and pathological features were obtained from medical records. Serum levels including high-density lipoprotein-cholesterol (HDL-c), low-density lipoprotein-cholesterol (LDL-c), total cholesterol (TC), triglyceride (TG), apolipoprotein A (ApoA), ApoB, ApoE and lipoprotein a(LP(a)) were collected before treatment. Logistic regression analyses were used to show the association between serum lipids and subtypes of BC. Receiver operating characteristic (ROC) curves were generated to analyze the predictive performance.ResultsThere were 70 ER-negative and 73 PR-negative BC. Patients with ER-negative BC had higher HDL-c, higher LDL-c, and higher LP(a) than those in ER-positive one (p < 0.05). Patients with PR-negative BC were more likely to have high LDL-c and high LP(a) levels than patients with PR-positive one (p < 0.05). Multivariate logistic regression analysis showed that serum HDL-c (odds ratio (OR): 0.27, 95% confidence interval (CI) 0.10–0.76), LDL-c (OR: 0.19, 95%CI 0.04–0.93) and LP(a) (OR: 0.23,95%CI 0.07–0.80) levels were negatively associated with ER-positive BC, and serum HDL-c and LDL-c levels were significantly negatively associated with PR-positive BC (OR: 0.32, 95%CI 0.12–0.82; OR: 0.14, 95%CI 0.03–0.77). In addition, ER and PR positive BC was negatively associated with serum HDL-c and LDL-c levels (OR = 0.39, 95% CI 0.17–0.91; OR = 0.22, 95% CI 0.06–0.85) after adjusting with confounders. Serum HDL-c level (OR = 0.13, 95% CI 0.02–0.87) was still independently associated with ER and PR positive BC in postmenopausal women. The area under the curves (AUCs) of HDL-c to identify ER-positive BC, PR-positive BC, and ER and PR positive BC were 0.65 (95%CI 0.58–0.73, P < 0.01), 0.62 (95%CI 0.54–0.69, P < 0.01) and 0.64 (95%CI 0.56–0.72, P < 0.01), respectively.ConclusionsSerum HDL-c and LDL-c levels were related to ER or PR positive BC. Lipid levels may also have acceptable performance in identifying BC histological type.

Sex differences in prevalence and clinical correlates of insomnia in Chinese patients with chronic schizophrenia.

It is generally recognized that there are sex differences in many aspects of schizophrenia. The main purpose of this study was to investigate the sex differences in the prevalence and clinical correlates of insomnia in patients with chronic schizophrenia. A total of 957 patients who met the DSM-IV diagnostic criteria for schizophrenia were recruited in this cross-sectional study (male/female = 630/327). Demographic, clinical, and insomnia data were collected using self-reported questionnaires. Fasting blood samples were collected to evaluate the status of blood lipids. Psychopathological symptoms were evaluated using the Positive and Negative Syndrome Scale (PANSS). The prevalence rate of insomnia in female patients with schizophrenia was significantly higher than that in male patients (17.3% for males and 26.3% for females; χ2 = 10.74, p = 0.001). Regression analysis showed that in male patients, insomnia was independently associated with severe PANSS positive symptoms, severe PANSS depressive factor, and high levels of low-density lipoprotein levels, while in female patients, insomnia was associated with low education level, high PANSS depressive factor, and high levels of apolipoprotein B levels. This study illustrates that insomnia is more frequent in female than male schizophrenia patients, and that there are differences in the clinical correlates of insomnia by sex, suggesting that sex differences should be considered in prevention and treatment strategies for coexisting insomnia in schizophrenia patients.

Association between serum zinc level and lipid profiles in children with spinal muscular atrophy.

Background and aimsChildren with spinal muscular atrophy (SMA) have a high rate of dyslipidaemia, which is a risk factor of vital importance for cardiovascular diseases in adulthood. Studies have demonstrated that the serum zinc level is associated with lipid profiles in the general population as well as in individuals diagnosed with obesity or diabetes. The purpose of this study was to evaluate the relationship between serum zinc level and lipid profiles in children with SMA.MethodsThis cross-sectional study was launched in a tertiary children's medical center in China and involved pediatric patients with SMA under the management of a multidisciplinary team of outpatient services from July 2019 to July 2021. Anthropometric information, general clinical data, serum zinc level, lipid profiles, and body composition data were collected. Multivariate analysis was used for a thorough inquiry on the association between the serum zinc level and lipid profiles.ResultsAmong the 112 patients with SMA [median (IQR) age 5.54 years (2.75–8.29), 58.04% female], who fulfilled the inclusion criteria of the study, dyslipidaemia was detected in 60 patients (53.57%). Based on multivariable linear regression, serum zinc level was positively associated with high-density lipoprotein cholesterol (HDL-C; β = 1.63, 95% CI = 0.44–3.22) and apolipoprotein A1 (APO A1; β = 2.94, 95% CI = 0.03–5.85) levels, independently of age, sex, type, activity, percentage of body fat, and body mass index. As the serum zinc level increased by 10 μmol/L, the risk of low APO A1 levels decreased by 35% (OR = 0.65, 95% CI = 0.44–0.97) according to multivariable logistic regression analyses.ConclusionSerum zinc concentration was positively correlated with HDL-C and APO A1 levels among children with SMA. We suggest measures to correct the lower level of serum zinc to improve HDL-C and APO A1 levels.

Portulaca oleracea L. Extract Regulates Hepatic Cholesterol Metabolism via the AMPK/MicroRNA-33/34a Pathway in Rats Fed a High-Cholesterol Diet.

This study examined the effect of extruded Portulaca oleracea L. extract (PE) in rats fed a high-cholesterol diet through the AMP-activated protein kinase (AMPK) and microRNA (miR)-33/34a pathway. Sprague–Dawley rats were randomized into three groups and fed either a standard diet (SD), a high-cholesterol diet containing 1% cholesterol and 0.5% cholic acid (HC), or an HC diet containing 0.8% PE for 4 weeks. PE supplementation improved serum, liver, and fecal lipid profiles. PE upregulated the expression of genes involved in cholesterol efflux and bile acids’ synthesis such as liver X receptor alpha (LXRα), ATP-binding cassette subfamily G5/G8 (ABCG5/8), and cholesterol 7 alpha-hydroxylase (CYP7A1), and downregulated farnesoid X receptor (FXR) in the liver. In addition, hepatic gene expression levels of apolipoprotein A-l (apoA-1), paraoxonase 1 (PON1), ATP-binding cassette subfamily A1/G1 (ABCA1/G1), lecithin-cholesterol acyltransferase (LCAT), and scavenger receptor class B type 1 (SR-B1), which are related to serum high-density lipoprotein cholesterol metabolism, were upregulated by PE. Furthermore, hepatic AMPK activity in the PE group was higher than in the HC group, and miR-33/34a expression levels were suppressed. These results suggest that PE improves the cholesterol metabolism by modulating AMPK activation and miR-33/34a expression in the liver.

Lipid levels in midlife and risk of atrial fibrillation over 3 decades-Experience from the Swedish AMORIS cohort: A cohort study.

BackgroundThe role of cholesterol levels in the development of atrial fibrillation (AF) is still controversial. In addition, whether and to what extent apolipoproteins are associated with the risk of AF is rarely studied. In this study, we aimed to investigate the association between blood lipid levels in midlife and subsequent risk of new-onset AF.Methods and findingsThis population-based study included 65,136 individuals aged 45 to 60 years without overt cardiovascular diseases (CVDs) from the Swedish Apolipoprotein-Related Mortality Risk (AMORIS) cohort. Lipids were measured in 1985 to 1996, and individuals were followed until December 31, 2019 for incident AF (i.e., study outcome). Hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated using Cox regression, adjusting for age, sex, and socioeconomic status. Over a mean follow-up of 24.2 years (standard deviation 7.5, range 0.2 to 35.9), 13,871 (21.3%) incident AF cases occurred. Higher levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) were statistically significantly associated with a lower risk of AF during the first 5 years of follow-up (HR = 0.61, 95% CI: 0.41 to 0.99, p = 0.013; HR = 0.64, 95% CI: 0.45 to 0.92, p = 0.016), but not thereafter (HR ranging from 0.94 [95% CI: 0.89 to 1.00, p = 0.038] to 0.96 [95% CI: 0.77 to 1.19, p > 0.05]). Lower levels of high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (ApoA-I) and higher triglycerides (TG)/HDL-C ratio were statistically significantly associated with a higher risk of AF during the entire follow-up (HR ranging from 1.13 [95% CI: 1.07 to 1.19, p < 0.001] to 1.53 [95% CI: 1.12 to 2.00, p = 0.007]). Apolipoprotein B (ApoB)/ApoA-I ratio was not associated with AF risk. The observed associations were similar among those who developed incident heart failure (HF)/coronary heart disease (CHD) and those who did not. The main limitations of this study include lack of adjustments for lifestyle factors and high blood pressure leading to potential residual confounding.ConclusionsHigh TC and LDL-C in midlife was associated with a lower risk of AF, but this association was present only within 5 years from lipid measurement and not thereafter. On the contrary, low HDL-C and ApoA-I and high TG/HDL-C ratio were associated with an increased risk of AF over almost 35 years of follow-up. ApoB/ApoA-I ratio was not associated with AF risk.

Interleukin 1 receptor antagonist relation to cardiovascular disease risk in patients with rheumatoid arthritis

Interleukin (IL) 1, and its family member, IL-1 receptor antagonist (IL-1ra), are involved in the pathogenesis and inflammation perpetuation of patients with rheumatoid arthritis (RA). Besides, IL-1 has been linked to an increased risk and greater severity of cardiovascular (CV) disease. We aimed to study if IL-1ra is related to the CV manifestations—including lipid pattern and insulin resistance or subclinical atherosclerosis—that accompanies the disease in a large series of patients with RA. Cross-sectional study that encompassed 430 patients with RA. Serum IL-1ra levels were assessed. A multivariable analysis was performed to analyze the relation of IL-1ra to subclinical carotid atherosclerosis, and to traditional CV factors including a complete lipid molecules profile and insulin resistance or beta cell function indices. Body mass index, abdominal circumference, and the presence of obesity were significantly and positively associated with circulating IL-1ra. Similarly, erythrocyte sedimentation rate, and disease activity scores were significantly related to higher IL-1ra serum levels after adjustment for confounders. Neither carotid intima-media thickness nor the presence of carotid plaque were associated with serum levels of IL-1ra. However, after multivariable analysis circulating IL-1ra was independently and positively associated with higher serum levels of total cholesterol, triglycerides, and apolipoproteins B and C-III. Similarly, IL-1ra was related to higher levels of beta-cell function in the univariable analysis, although, in this case, significance was lost after adjustment. Among patients with RA, IL-1ra is associated with both disease activity and several traditional CV risk factors such as obesity and the presence of higher lipid levels. Our findings suggest that IL-1ra can represent a link between the inflammation and the CV disease risk that are present in patients with RA.

Long-Term Alcohol Consumption Caused a Significant Decrease in Serum High-Density Lipoprotein (HDL)-Cholesterol and Apolipoprotein A-I with the Atherogenic Changes of HDL in Middle-Aged Korean Women.

Light-to-moderate alcohol drinking is associated with a low incidence of cardiovascular disease (CVD) via an elevation of high-density lipoproteins-cholesterol (HDL-C), particularly with the short-term supplementation of alcohol. However, there is no information on the change in the HDL qualities and functionalities between non-drinkers and mild drinkers in the long-term consumption of alcohol. This study analyzed the lipid and lipoprotein profiles of middle-aged Korean female non-drinkers, mild-drinkers, and binge-drinkers, who consumed alcohol for at least 10 years. Unexpectedly, the serum levels of HDL-C and apolipoprotein A-I (apoA-I) were decreased significantly depending on the alcohol amount; the binge-drinker group showed 18% and 13% lower HDL-C (p = 0.011) and apoA-I levels (p = 0.024), respectively, than the non-drinker group. Triglyceride (TG) and oxidized species, malondialdehyde (MDA), and low-density lipoproteins (LDL) levels were significantly elevated in the drinker groups. Interestingly, the binge-drinker group showed 1.4-fold higher (p = 0.020) cholesterol contents in HDL2 and 1.7-fold higher (p < 0.001) TG contents in HDL3 than those of the non-drinker group. The mild-drinker group also showed higher TG contents in HDL3 (p = 0.032) than the non-drinker group, while cholesterol contents were similar in the HDL3 of all groups. Transmission electron microscopy (TEM) showed that the non-drinker group showed a more distinct and clear particle shape of the LDL and HDL image with a larger particle size than the drinker group. Electrophoresis of LDL showed that the drinker group had faster electromobility with a higher smear band intensity and aggregation in the loading position than the non-drinker group. The HDL level of binge drinkers showed the lowest paraoxonase activity, the highest glycated extent, and the most smear band intensity of HDL and apoA-I, indicating that HDL quality and functionality were impaired by alcohol consumption. In conclusion, long-term alcohol consumption in middle-aged women, even in small amounts, caused a significant decrease in the serum HDL-C and apoA-I with atherogenic changes in LDL and HDL, such as an increase in TG and MDA content with a loss of paraoxonase activity.

Cluster of Differentiation 147 (CD147) serves as a promoter of atherosclerosis in patients with cerebral infarction.

The aim of this study was to investigate the correlations of cluster of differentiation 147 (CD147) with plaque stability of carotid atherosclerosis (AS), degree of stenosis, inflammatory factors, matrix metalloproteinase-9 (MMP-9) expression and vascular endothelial function in patients with cerebral infarction. A total of 50 patients diagnosed with cerebral infarction (cerebral infarction group), 70 patients diagnosed with AS plaque (plaque group, with no infarction but plaques only) and 30 healthy people receiving physical examination (control group) in our hospital from March 2018 to July 2019 were collected. The levels of biochemical indexes, CD147, MMP-9, vascular endothelial function indexes [endothelin-1 (ET-1) and C-reactive protein (CRP)] and inflammatory factors [interleukin-10 (IL-10), IL-16 and tumor necrosis factor-alpha (TNF-α)] in the blood of each group of patients were detected via radioimmunoassay and enzyme-linked immunosorbent assay (ELISA). Moreover, ultrasonic examination and Gensini score system were applied to score the degree of carotid stenosis in cerebral infarction group. Finally, the differences in various parameters were compared among the three groups, and the correlations of CD147 with different indexes were evaluated using Spearman method. Compared with those in control group, the levels of CD147, MMP-9, hemoglobin, platelets, total cholesterol, triglyceride, low-density lipoprotein (LDL), high-density lipoprotein (HDL), apolipoprotein A, apolipoprotein B, IL-10, IL-13 and TNF-α in the blood were remarkably elevated in cerebral infarction group and plaque group (p<0.05). Cerebral infarction group had notably higher levels of CD147, hemoglobin, triglyceride, apolipoprotein B, IL-10, IL-13 and TNF-α in the blood than plaque group (p<0.05). The plaque score was markedly higher in cerebral infarction group than that in plaque group [(3.27±2.86) points vs. (0.93±1.44) points] (p<0.05). In comparison with control group, plaque group and cerebral infarction group exhibited evidently raised levels of blood ET-1 and CRP (p<0.05). The serum CD147 level was significantly associated with MMP-9 (p=0.003, r=0.616), Gensini score (p=0.006, r=0.656), plaque score (p=0.027, r=0.396), IL-10 (p=0.004, r=0.603), TNF-α (p=0.001, r=0.746) and CRP (p=0.037, r=0.450) in cerebral infarction group. CD147 level is prominently increased in carotid AS and closely related to inflammatory responses, and CD147 may become a new reference for the prediction and treatment of AS and cerebral infarction.