Search

The study examined the impact of Salicornia supplementation on the biological efficiency and biochemical properties of white Elm oyster mushrooms, Hypsizygus ulmarius. Four substrates were used to cultivate the mushrooms. Wheat straw was used as the main substrate and the Salicornia was used to partially replace the main substrate at the ratios of 5, 10, and 20% while 100% wheat straw was used as the control. The study found that the 20% Salicornia completed the mycelial run earlier (41 days), while the control treatment took the longest (45 days). The 5% Salicornia supplemented treatment and control treatment had the highest and lowest biological efficiencies (126 and 65%) respectively. The elemental concentration was undetectable for Copper (Cu), Lead (Pb), and Cadmium (Cd). The mushrooms from the control had the highest while those from the 20% treatment had the lowest (Zinc (Zn) levels (0.0115 ug/100 g) and 0.0078 ug/100 g). Conversely, Chromium (Cr) levels were highest and lowest in the 20% (0.0022 ug/100 g) and control treatments (0.0007 ug/100 g). Similarly, the total unsaturated fatty acids were highest in the control treatment (78%) and lowest in the 20% treatment (69%) while the opposite was true for the saturated fatty acids (22% and 31%). The mushrooms investigated in this study had higher essential amino acids (44–49%) compared to non-essential amino acids (17–20%). The results from this study suggest that Salicornia is a promising marine resource with the potential to enhance the health-promoting properties of oyster mushrooms. [ABSTRACT FROM AUTHOR]

Background. Diabetes mellitus causes fasting hyperglycemia and dyslipidemia, and exposure of diabetics to aluminium can aggravate these effects, since aluminium exposure also causes prediabetic hyperglycemia and dyslipidemia. The effect has not been previously demonstrated in an animal model. Aim. Objective of the study was to determine the extent of aggravation of dyslipidemia after subchronic oral exposure of diabetics (type 1 model in rat) to aluminium chloride.Method. Forty adult male rats (weighing 189–285 g) were divided into four groups of ten rats each: Control group (CG); Aluminium chloride (Al) treated group (AG); Diabetic group (DG); Al-treated-diabetic group (ADG). Diabetes was induced by single intramuscular injection of aqueous alloxan monohydrate (100 mg/ml) at 120 mg/kg in DG and ADG. Each rat in the Al-treated groups (AG and ADG) was orally administered with aqueous aluminium chloride (100 g/L) daily (50 mg/kg; 12.5% of LD50) by gavage for 28 days. Fasting blood glucose (FBG) and serum total cholesterol (TC), triglyceride (TG) and high density lipoprotein cholesterol (HDLc) concentrations were determined. Low density lipoprotein cholesterol (LDLc) and atherogenic index of plasma (AIP) were calculated with formulae. Results. Diabetic hyperglycemia was maintained in DG and did not differ from ADG on day 7–21, but was higher (p < 0.05) on day 28 in association with aggravated dyslipidemia characterized by increases in TG, TC, LDLc, AIP and decrease in HDLc. Conclusion. Subchronic aluminium exposure in diabetics aggravated hyperglycemia and dyslipidemia with AIP elevation by 34%, suggesting an exaggeration of risk of atherogenesis, atherosclerosis and cardiovascular disease. [ABSTRACT FROM AUTHOR]

Half of dyslipidemic patients sometimes discontinue statin medication. It is unclear if blood atherogenic risk increases right after statin discontinuation or if there is a lingering protective effect. We sought to determine if a legacy effect prevented blood lipid increases during the first stages of statin cessation. Atherogenic blood lipid profile was measured in 10 overweight (BMI 31 ± 3 kg m−2) middle-aged males (62 ± 7 years old), statin users, while fasted and postprandially. Trials were conducted before (i.e., Day 0) and after 4, 7, 15, and 30 days of statin withdrawal and 20 days after statins reloading (Day 50). Four days after statin discontinuation, blood fasting LDL-c, total cholesterol (CHOL), and triglyceride (TG) concentrations increased by 30%, 18%, and 17%, respectively (P < 0.05). The increases in LDL-c, CHOL, and TG peaked after 7–15 days at 79%, 48%, and 34% of basal levels (P < 0.001), respectively. There were no significant correlations between the increases in blood lipids and the dose or years under statin treatment (P = 0.156–0.575). Twenty days after resuming statins, blood LDL-c (2.79 ± 1.06 vs 2.20 ± 0.50 mmol L−1; P = 0.568), CHOL (4.85 ± 1.41 vs 4.25 ± 0.83 mmol L−1; P = 0.747), and TG (1.47 ± 0.60 vs 1.50 ± 0.68 mmol L−1; P = 0.782), returned to basal levels. Our data does not support a statin lingering/legacy effect in blood lipids since they dangerously increased after only 4 days of statin withdrawal in every patient, regardless of dose and years under treatment. Reloading statins restored blood lipids, evidencing a reproducible biological effect at the whole-body level. [Display omitted] • Up to 50% of patients discontinue statin medication for short periods feeling protected by a lingering pharmacological effect. • We discontinued statins for 30 days in ten dyslipidemic patients, while monitoring their blood lipid profile. • LDL-c increased linearly at rates of 0.13 mmol·L−−1·day −1 independently of previous length or dose of statin prescription. • We found no evidence of a statin lingering effect once discontinued. Luckily, statin reintroduction quickly reversed the dyslipidemia. [ABSTRACT FROM AUTHOR]

Abstract The study examined the impact of Salicornia supplementation on the biological efficiency and biochemical properties of white Elm oyster mushrooms, Hypsizygus ulmarius. Four substrates were used to cultivate the mushrooms. Wheat straw was used as the main substrate and the Salicornia was used to partially replace the main substrate at the ratios of 5, 10, and 20% while 100% wheat straw was used as the control. The study found that the 20% Salicornia completed the mycelial run earlier (41 days), while the control treatment took the longest (45 days). The 5% Salicornia supplemented treatment and control treatment had the highest and lowest biological efficiencies (126 and 65%) respectively. The elemental concentration was undetectable for Copper (Cu), Lead (Pb), and Cadmium (Cd). The mushrooms from the control had the highest while those from the 20% treatment had the lowest (Zinc (Zn) levels (0.0115 ug/100 g) and 0.0078 ug/100 g). Conversely, Chromium (Cr) levels were highest and lowest in the 20% (0.0022 ug/100 g) and control treatments (0.0007 ug/100 g). Similarly, the total unsaturated fatty acids were highest in the control treatment (78%) and lowest in the 20% treatment (69%) while the opposite was true for the saturated fatty acids (22% and 31%). The mushrooms investigated in this study had higher essential amino acids (44–49%) compared to non-essential amino acids (17–20%). The results from this study suggest that Salicornia is a promising marine resource with the potential to enhance the health-promoting properties of oyster mushrooms.

Cardiovascular disease is prevalent globally and is the most common complication of metabolic syndrome (MetS). Previous studies have suggested that curcumin and probiotics may improve the lipid profile, so we aimed to investigate the effects of the edible powder enriched with these substances on lipid profile level and atherogenic indices such as Atherogenic Coefficient (AC), Castelli Risk Index‐I (CRI‐I), Castelli Risk Index‐II (CRI‐II), and Atherogenic Index of Plasma (AIP). In the present parallel randomized double‐blinded placebo‐controlled clinical trial, 124 people with MetS with overweight or obesity were randomly allocated to 4 groups and were followed up for 8 weeks. The participants received a low‐calorie diet and a daily sachet of enriched powder drink. The sachets contained either 109 CFU of probiotics or 1 g of curcumin, or probiotic + curcumin (pro + cur), or placebo, respectively. The fasting lipid profile and atherogenic indices were measured at the beginning and end of the study. One hundred and fourteen participants completed the study. At the end of the study, the within‐ and between‐group comparisons showed no significant differences in lipid profile and atherogenic indices (p >.05). Based on the results of the current study, taking an oral powder containing 1 g curcumin and 109 CFU probiotics for 8 weeks had no effect on the lipid profile level and atherogenic indices; however, more studies are recommended. [ABSTRACT FROM AUTHOR]

Elevated lipoprotein(a) (Lp[a]) is an independent, genetic risk factor for atherosclerotic cardiovascular disease (ASCVD) that impacts ~1.4 billion people globally. Generally, Lp(a) levels remain stable over time; thus, most individuals need only undergo Lp(a) testing through a non-fasting blood draw once in their lifetime, unless elevated Lp(a) is identified. Despite the convenience of the test for clinicians and patients, routine Lp(a) testing has not been widely adopted. This review provides a guide to the benefits of Lp(a) testing and solutions for overcoming common barriers in practice, including access to testing and lack of awareness. Lp(a) testing provides the opportunity to reclassify ASCVD risk and drive intensive cardiovascular risk factor management in individuals with elevated Lp(a), and to identify patients potentially less likely to respond to statins. Moreover, cascade screening can help to identify elevated Lp(a) in relatives of individuals with a personal or family history of premature ASCVD. Overall, given the profound impact of elevated Lp(a) on cardiovascular risk, Lp(a) testing should be an essential component of risk assessment by primary and specialty care providers.

Background: Lannea egregia leaf has been used locally for the management of diseases with limited scientific support. Hence, the cardiomyopathy protective ability of an alkaloid-rich extract of L. egregia leaf in streptozotocin-induced type 2 diabetic rats was investigated in this study. A L. egregia leaf alkaloid-rich extract was obtained using a standard procedure. Streptozotocin was injected into the experimental animals intraperitoneal at a dose of 45 mg/kg body weight to induce type 2 diabetes mellitus, prior to this, the animals were given 20 % (w/v) fructose for one week. Thus, the animals were grouped into five (n = 8), comprising normal control (NC), diabetic control (DC), diabetic rats treated with low (50 mg/kg body weight) and high (100 mg/kg body weight) doses of L. egregia alkaloid-rich leaf extracts (i.e., LEL and LEH, respectively), and 200 mg/kg body weight metformin (MET). The animals were sacrificed on the 21st day, and blood and hearts were harvested and used for the determination of serum lipid profiles, atherogenic indices, oxidative stress biomarkers, ATPase activities, cardiac enzyme activities, creatinine kinase-MB, cardiac troponin, cytokines, N-terminal pro-B-type brain natriuretic peptide (NT-pro BNP) and histology examination. Results: The results revealed that diabetic rats treated with LEL, LEH, and MET significantly (p

Copyright of Revista Latinoamericana de Hipertension is the property of Revista Latinoamericana de Hipertension and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction Endoplasmic reticulum plays an essential role in many cellular pathways. Exercise and fasting can lead to liver health by activating mechanisms such as reticulophagy. Therefore, the aim of the current research is to investigate the effect of fasting and aerobic exercise on atherogenic indicators, body mass and ATF6 gene expression in the endoplasmic reticulum of healthy liver of Wistar rats. Material and Method In this experimental research, 30 Wistar rats (18 weeks old) with a weight range of 330.40 ± 25.34 grams were selected and divided into six groups: 1) control 2) starvation 3) 3 days of training 4) 5 days of training 5) 3 Day of training + starvation 6) 5 days of training + starvation were divided. The rats in the training group trained on the treadmill for one month, 3 and 5 sessions a week for one hour. Starvation was for 14 hours when the rats were awake, which was done continuously for one month. Data analysis was performed using one-way ANOVA and post hoc LSD statistical tests in SPSS version 23 software. A significance level of P≥0.05 was considered. Results Data analysis showed a significant decrease in BMI, LDL/HDL, CHOL/HDL, TAG/HDL and a significant increase in ATF6 gene expression (P≥0.05). Conclusion Aerobic training with starvation led to liver health by reducing atherogenic indicators. Also, increasing the expression of ATF6 gene in the liver through exercise and starvation can lead to the regulation of reticulophagia and liver health. [ABSTRACT FROM AUTHOR]

Grewia mollis Juss (Malvaceae) commonly described as "Dargaza" is a shrub, popularly used in folk medicine to treat obesity, diarrhoea and to ease childbirth. However, there are no established reports on its antiobesity activity in literature, hence, the aim of the study was to evaluate the antihyperlipidemic and antiobesity effects of Grewia mollis (GM) in rodents. Hyperlipidemia was induced by 200 mg/kg of triton WR-1339 and the rats were orally pretreated with extract (150-600 mg/kg) and atorvastatin (25 mg/kg) for 3 days. Obesity was induced with dietary cholesterol (600 mg/kg) for 10 weeks and rats were orally treated with extract (150-600 mg/kg). The effects of the extract on body weight, total food consumption, relative organ weight, Lee index, lipid profile, atherogenic index, coronary risk index and histopathological indices were evaluated. Preliminary phytochemical screening showed presence tannins, saponins, alkaloids, flavonoids and steroidal nucleus. The extract significantly (p<0.05) decreased total cholesterol, triglyceride, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol (VLDL), non-high-density lipoprotein cholesterol, atherogenic index, coronary risk index in hyperlipidemic rats. In the obese rat, there was significant (p<0.05) decrease in relative liver weight, body weight, Lee index, triglycerides, VLDL. Atherosclerotic changes in the coronary artery and aorta were ameliorated by the extract. The reduction in lipid profile and amelioration of atherosclerotic lesions indicate a possible anti-atherogenic property. These effects appear to be mediated via inhibition de novo triglyceride and cholesterol biosynthesis. The extract shows therapeutic promise in the management of obesity, hyperlipidemia and in the prevention of atherosclerosis. [ABSTRACT FROM AUTHOR]

The aim of this study was to determine the effect of olive oil addition on the production, chemical composition, and fatty acid profile of sheep's milk. Twenty-four lactating ewes with a live weight of 34.6 ± 4.61 kg were used. The animals were randomly distributed into four treatments (n = 6) with dietary addition of 0%, 2%, 4%, and 6% (dry matter basis) olive oil for 45 days. Milk samples were taken every 7 days for fatty acid (FA) and chemical analyses. A decrease (p < 0.05) in dry matter and crude protein intake was observed with 4% oil inclusion. Milk production and milk components were similar between treatments. The kilograms of meat from weaned lambs linearly increased as the oil inclusion increased. Milk C4:0 to C17:0 decreased with 2% olive oil. The monounsaturated and polyunsaturated FA content in the milk increased with the oil inclusion. There was an increase in the milk's linoleic acid, linolenic acid, and eicosapentaenoic acid content with 2% olive oil. Overall, the addition of 2% extra virgin olive oil is recommended to improve milk's FA profile without negative effects on animal performance. [ABSTRACT FROM AUTHOR]

Background: Recent research has demonstrated the possible relevance of bilirubin in metabolic and cardiovascular disorders. Lipid abnormalities are a major problem that is related with an increased risk of cardiovascular disease in diabetics. This study examined the relationship between serum bilirubin and direct bilirubin concentrations and atherogenic lipids in patients with type 2 diabetes (T2DM). Methods: This cross-sectional included 67 patients with type 2 diabetes and 39 matched healthy control. The lipid profile, including total cholesterol, HDL-C, and TG levels, fasting blood glucose, total bilirubin, direct bilirubin, ALT, AST, and ALP were measured using a dimension EXL clinical chemistry analyzer (Siemens Healthcare Diagnostics). Cholesterol in VLDL, LDL, and sdLDL were calculated from standard lipid assay results by the equations of Sampson et al. Results: Serum bilirubin was lower in non T2DM subjects nearly significant (p=0.0.51) whereas direct bilirubin concentrations were lower in T2DM (p=0.008). ALT, AST, and ALP levels were higher in T2DM groups. The mean values of LDL-C, sdLDL-C, non HDL-C and VLDL-C were significantly increased in T2DM group and lower HDL-C. An inverse relationship could be observed with increase in serum total bilirubin and serum levels of LDL-C (r2=0.139, p<0.005), sdLDL-C (r2=0.137, p<0.005), VLDL-C (r2=0.074, p<0.044), and non HDL-C (r2=0.166, p<0.002) in T2DM group. The same inverse relationship was observed with serum direct bilirubin and serum levels of LDL-C (r2=0.133, p<0.006), sdLDL-C (r2=0.172, p<0.001), VLDL-C (r2=0.118, p<0.01), and non HDL-C (r2=0.182, p<0.001) in T2DM group. Conclusions: A significant negative association was found between serum bilirubin levels and direct serum bilirubin with atherogenic lipids, suggesting that serum bilirubin may protect T2DM patients from development of cardiovascular disease. These findings indicate the need for additional research in a large cohort. [ABSTRACT FROM AUTHOR]

IntroductionAtherosclerosis is a progressive disease that develops in areas of disturbed flow (d-flow). Progressive atherosclerosis is characterized by bulky plaques rich in mesenchymal cells and high-grade inflammation that can rupture leading to sudden cardiac death or acute myocardial infarction. In response to d-flow, endothelial cells acquire a mesenchymal phenotype through endothelial-to-mesenchymal transition (EndMT). However, the signaling intermediaries that link d-flow to EndMT are incompletely understood.Methods and ResultsIn this study we found that in human atherosclerosis, cells expressing SNAI1 (Snail 1, EndMT transcription factor) were highly expressed within the endothelial cell (EC) layer and in the pre-necrotic areas in unstable lesions, whereas stable lesions did not show any SNAI1 positive cells, suggesting a role for EndMT in lesion instability. The interleukin-1 (IL-1), which signals through the type-I IL-1 receptor (IL-1R1), has been implicated in plaque instability and linked to EndMT formation in vitro. Interestingly, we observed an association between SNAI1 and IL-1R1 within ECs in the unstable lesions. To establish the causal relationship between EndMT and IL-1R1 expression, we next examined IL-1R1 levels in our Cre-lox endothelial-specific lineage tracing mice. IL-1R1 and Snail1 were highly expressed in ECs under atheroprone compared to athero-protective areas, and oscillatory shear stress (OSS) increased IL-1R1 protein and mRNA levels in vitro. Exposure of ECs to OSS resulted in loss of their EC markers and higher induction of EndMT markers. By contrast, genetic silencing of IL-1R1 significantly reduced the expression of EndMT markers and Snail1 nuclear translocation, suggesting a direct role for IL-1R1 in d-flow-induced EndMT. In vivo, re-analysis of scRNA-seq datasets in carotid artery exposed to d-flow confirmed the IL-1R1 upregulation among EndMT population, and in our partial carotid ligation model of d-flow, endothelial cell specific IL-1R1 KO significantly reduced SNAI1 expression.DiscussionGlobal inhibition of IL-1 signaling in atherosclerosis as a therapeutic target has recently been tested in the completed CANTOS trial, with promising results. However, the data on IL-1R1 signaling in different vascular cell-types are inconsistent. Herein, we show endothelial IL-1R1 as a novel mechanosensitive receptor that couples d-flow to IL-1 signaling in EndMT.

Men and women differ in circulating lipids and coronary artery disease (CAD). While sex hormones such as estrogens decrease CAD risk, hormone replacement therapy increases risk. Biological sex is determined by sex hormones and chromosomes, but effects of sex chromosomes on circulating lipids and atherosclerosis are unknown. Here, we use mouse models to separate effects of sex chromosomes and hormones on atherosclerosis, circulating lipids and intestinal fat metabolism. We assess atherosclerosis in multiple models and experimental paradigms that distinguish effects of sex chromosomes, and male or female gonads. Pro-atherogenic lipids and atherosclerosis are greater in XX than XY mice, indicating a primary effect of sex chromosomes. Small intestine expression of enzymes involved in lipid absorption and chylomicron assembly are greater in XX male and female mice with higher intestinal lipids. Together, our results show that an XX sex chromosome complement promotes the bioavailability of dietary fat to accelerate atherosclerosis.

Abstract Background Patients with non-alcoholic fatty liver disease (NAFLD) as well as type 2 diabetes mellitus (T2DM) are at increased risk for cardiovascular diseases (CVD). Omega-3 supplementation has been proposed as a possible strategy for management of cardiometabolic risk. Cardiometabolic indices can predict and evaluate the cardiometabolic risk. Aims We investigated the effect of omega-3 supplementation on accurate and available cardiometabolic indices including atherogenic index of plasma (AIP), Castelli risk index I, Castelli risk index II and atherogenic coefficient (AC) in diabetic patients with NAFLD. Methods We conducted a double-blind, randomized controlled trial (RCT) for 12 weeks. From August 2016 to March 2017, the subjects referred to Faghihi hospital in Shiraz, Iran, were recruited. Sixty diabetic patients with NAFLD were randomly assigned into the omega-3 (2000 mg/d omega-3 capsule contained 360 mg/d eicosapentaenoic acid and 240 mg/d docosahexaenoic acid) and the placebo (liquid paraffin) groups using computer-generated random number table. Results Omega-3 supplementation compared to the placebo had no significant effect on AIP (− 0.11 ± 0.20 vs. -0.03 ± 0.16; P = 0.11), Castelli risk index I (− 0.25 ± 0.6 vs. -0.07 ± 0.7; P = 0.42), Castelli risk index II (− 0.24 ± 0.5 vs. -0.14 ± 0.5; P = 0.63) and AC (− 0.25 ± 0.6 vs. -0.07 ± 0.7; P = 0.42). After adjusting for confounding factors, the findings remained without change. Conclusion Omega-3 supplementation (2000 mg/d) for 12 weeks has no effect on cardiometabolic risk. It seems, higher doses of omega-3 can improve cordiometabolic risk. The trial was registered at Iranian Registry of Clinical Trials IRCT2016102530489N1.

PurposeWe aimed to analyze the correlation between overweight and obesity-related indicators and cardiovascular risk predictors in patients with familial hypercholesterolemia (FH) and to evaluate their mutual predictive properties.MethodsA total of 103 patients with FH included from 2004 to 2017 were retrospectively analyzed. Pearson correlation analysis and multiple linear regression analysis were used to assess the correlation between overweight and obesity-related indicators and cardiovascular risk predictors in FH patients. Subject operating characteristic (ROC) curve was used to analyze their reciprocal predictive performance.Results(1) Atherogenic index of plasma (AIP) (β = 0.020) and ApoB/ApoA1 Ratio (BAR) (β = 0.015) were independently correlated with body mass index (BMI) (P < 0.05); AIP (β = 1.176) was independently correlated with waist-to-hip ratio (WHR) (P < 0.01); AIP (β = 1.575), BAR (β = 0.661) and atherogenic coefficient (AC) (β = 0.427) were independently correlated with waist-to-height ratio (WHtR) (P < 0.05). (2) The area under the ROC (AUC) for overweight corresponding to AIP, BAR, and AC were 0.695 (95% CI = 0.593–0.797, P < 0.01), 0.660 (95% CI = 0.555–0.766, P < 0.01), and 0.632 (95% CI = 0.525–0.740, P < 0.05), respectively; and AUCs for central obesity corresponding to AIP, BAR and AC were 0.757 (95% CI = 0.656–0.857, P < 0.001), 0.654 (95% CI = 0.536–0.771, P < 0.05) and 0.651 (95% CI = 0.538–0.764, P < 0.05), respectively. The AUCs for moderate risk of AIP corresponding to BMI, WHR, and WHtR were 0.709 (95% CI = 0.608–0.811, P < 0.001), 0.773 (95% CI = 0.678–0.867, P < 0.001), 0.739 (95% CI = 0.641–0.836, P < 0.001), respectively, and BMI, WHR and WHtR corresponded to an AUC of 0.691 (95% CI = 0.585–0.797, P < 0.01), 0.734 (95% CI = 0.632–0.835, P < 0.001), and 0.706 (95% CI = 0.603–0.810, P < 0.01) for high risk of AIP, respectively.ConclusionAIP has independent positive linear correlation with indicators related to overweight and obesity in FH patients; AIP has good predictive performance for overweight and obesity in FH patients, and WHR has good performance for identifying moderate and high risk of AIP in FH patients.

The aim of this study was to determine the effect of olive oil addition on the production, chemical composition, and fatty acid profile of sheep’s milk. Twenty-four lactating ewes with a live weight of 34.6 ± 4.61 kg were used. The animals were randomly distributed into four treatments (n = 6) with dietary addition of 0%, 2%, 4%, and 6% (dry matter basis) olive oil for 45 days. Milk samples were taken every 7 days for fatty acid (FA) and chemical analyses. A decrease (p < 0.05) in dry matter and crude protein intake was observed with 4% oil inclusion. Milk production and milk components were similar between treatments. The kilograms of meat from weaned lambs linearly increased as the oil inclusion increased. Milk C4:0 to C17:0 decreased with 2% olive oil. The monounsaturated and polyunsaturated FA content in the milk increased with the oil inclusion. There was an increase in the milk’s linoleic acid, linolenic acid, and eicosapentaenoic acid content with 2% olive oil. Overall, the addition of 2% extra virgin olive oil is recommended to improve milk’s FA profile without negative effects on animal performance.

Most cells involved in atherosclerosis release extracellular vesicles (EVs), which can carry bioactive substances to downstream tissues via circulation. We hypothesized that EVs derived from atherosclerotic plaques could promote atherogenesis in remote locations, a mechanism that mimics the blood metastasis of cancer. Ldlr gene knockout (Ldlr KO) rats were fed on a high cholesterol diet and underwent partial carotid ligation to induce local atherosclerosis. EVs were separated from carotid artery tissues and downstream blood of carotid ligation by centrifugation. MiRNA sequencing and qPCR were then performed to detect miRNA differences in EVs from rats with and without induced carotid atherosclerosis. Biochemical analyses demonstrated that EVs derived from atherosclerosis could increase the expression of ICAM-1, VCAM-1, and E-selectin in endothelial cells in vitro. EVs derived from atherosclerosis contained a higher level of miR-23a-3p than those derived from controls. MiR-23a-3p could promote endothelial inflammation by targeting Dusp5 and maintaining ERK1/2 phosphorylation in vitro. Inhibiting EV release could attenuate atherogenesis and reduce macrophage infiltration in vivo. Intravenously administrating atherosclerotic plaque-derived EVs could induce intimal inflammation, arterial wall thickening and lumen narrowing in the carotids of Ldlr KO rats, while simultaneous injection of miR-23a-3p antagomir could reverse this reaction. The results suggested that EVs may transfer atherosclerosis to remote locations by carrying proinflammatory factors, particularly miR-23a-3p. [ABSTRACT FROM AUTHOR]

Introduction: Scientific evidence suggests a reduction in the anti-atherogenic and antioxidant effects of paraoxonase-1 (PON1) in the presence of obesity. The aim of this study was to determine the effect of 8 weeks TRX on PON1 and HDL in inactive middle-aged obese women. Materials and Methods: For this purpose, 28 sedentary middle-aged obese women aged 30-40 years of old (30 ≤ BMI ≤ 36) were randomly divided into of TRX (8 weeks, 3days/weekly, n= 14) and control (no training, n = 14) groups. Fasting levels of PON1 and HDL and anthropometric indices (Weight, abdominal circumference, body mass index, visceral fat, body fat percentage) were measured before and 48 hours after lasted exercise session in both groups. Independent and paired t-test was used to compare baseline levels and changes in variables between the two groups before and after the training program. Results: TRX training led to a significant increase in PON1 (p= 0.016) a significant decrease in anthropometric indices (p < 0.05) and but HDL did not change significantly (p = 0.087). None of these variables were changed in the control group (p > 0.05). Conclusion: Despite no change in HDL, TRX training by increasing PON1 is associated with antioxidant and anti-atherogenic effects in obese middle-aged women. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the pattern of dyslipidaemia, risk factors, and comorbidities in young Indian adults with dyslipidaemia. Methods: A retrospective, multi-centric real-world study included individuals with dyslipidaemia, aged 18 - 45 years, attending to 623 hospitals/clinics across India. Data were collected retrospectively from medical records to note demographics, risk factors (smoking, alcohol consumption, sedentary lifestyle, family history of dyslipidaemia, diabetes mellitus, and hypertension), and clinical details (height, weight, waist circumference, body mass index (BMI), blood pressure, blood sugar, glycated hemoglobin (HbA1c), triglycerides (TG), total cholesterol (TC), low-density lipoproteins (LDL-C), and high-density lipoprotein (HDL-C)).A descriptive analysis and comparative analysis (Mann-Whitney U test and Chi-square test) were done. Results: Of the total 8135 patients, the majority were men (65.0%). Overall, 87.1% of population had one or multiple comorbidities which included the presence of dyslipidaemia alone (12.9%), dyslipidaemia with diabetes and hypertension (39.1%), dyslipidaemia with diabetes (33.6%), and dyslipidaemia with hypertension (14.4%). Sedentary lifestyle was prevalent observation in >50% of the population. Youngest age (18 - 25) group had higher prevalence of hypertriglyceridemia (63.2%), high LDL-C levels (56.8%), and low HDL-C levels (64.6%), while patients from the age group >25 to ≤35 years had the highest incidence of hypercholesterolemia (66.6%). Atherogenic dyslipidaemia was observed in 41.9%, 25.5%, and 23.2% of patients from age groups of ≥18 to ≤25, >25 to ≤35, and >35 to ≤45 years, respectively. Patients with HbA1c ≥6.5% had significantly higher levels of TG, TC, LDL-C, and lower HDL-C compared to those with HbA1c

Background: Patients with non-alcoholic fatty liver disease (NAFLD) as well as type 2 diabetes mellitus (T2DM) are at increased risk for cardiovascular diseases (CVD). Omega-3 supplementation has been proposed as a possible strategy for management of cardiometabolic risk. Cardiometabolic indices can predict and evaluate the cardiometabolic risk. Aims: We investigated the effect of omega-3 supplementation on accurate and available cardiometabolic indices including atherogenic index of plasma (AIP), Castelli risk index I, Castelli risk index II and atherogenic coefficient (AC) in diabetic patients with NAFLD. Methods: We conducted a double-blind, randomized controlled trial (RCT) for 12 weeks. From August 2016 to March 2017, the subjects referred to Faghihi hospital in Shiraz, Iran, were recruited. Sixty diabetic patients with NAFLD were randomly assigned into the omega-3 (2000 mg/d omega-3 capsule contained 360 mg/d eicosapentaenoic acid and 240 mg/d docosahexaenoic acid) and the placebo (liquid paraffin) groups using computer-generated random number table. Results: Omega-3 supplementation compared to the placebo had no significant effect on AIP (− 0.11 ± 0.20 vs. -0.03 ± 0.16; P = 0.11), Castelli risk index I (− 0.25 ± 0.6 vs. -0.07 ± 0.7; P = 0.42), Castelli risk index II (− 0.24 ± 0.5 vs. -0.14 ± 0.5; P = 0.63) and AC (− 0.25 ± 0.6 vs. -0.07 ± 0.7; P = 0.42). After adjusting for confounding factors, the findings remained without change. Conclusion: Omega-3 supplementation (2000 mg/d) for 12 weeks has no effect on cardiometabolic risk. It seems, higher doses of omega-3 can improve cordiometabolic risk. The trial was registered at Iranian Registry of Clinical Trials IRCT2016102530489N1. [ABSTRACT FROM AUTHOR]

Revive capsule is a polyherbal formulation commonly used to treat erectile dysfunction or enhance libido in men. This drug has similar mechanism of action with phosphodiesterase type-5 (PDE5) inhibitors. However, there have been speculations about the relationship between PDE5 inhibitors and cardiovascular disease, hence the need for this study, which was aimed at evaluating the effects of Revive capsule on cardiovascular risk indices in male albino rats in relation to the duration of administration. A total of 42 male albino rats were used for the study, and were divided into six (6) groups of seven (7) rats each. They were allowed to acclimatize for two (2) weeks by maintaining 12-hour light and dark cycles daily, with access to standard feed and water ad libitum. Group I (Negative Control group) was administered with distilled water once daily, while groups II, III, IV, V and VI were treated with Revive capsule at a dosage of 72mg/kg once daily for 1 week, 2 weeks, 3 weeks, 4 weeks and 6 weeks respectively. The rat dose administered was extrapolated from the human dose using the formula by Paget and Barnes. At the end of each treatment week, the rats were allowed to fast overnight, followed by their anaesthetization using chloroform, and blood sample collection via jugular vein puncture. Also, the heart was excised and examined histologically. Fasting lipid profile total cholesterol, triglycerides and high density lipoprotein was analyzed using Randox test kits with enzymatic method; the low density lipoprotein was calculated using Friedewald's equation; then, the cardiovascular (atherogenic) risk indices were calculated using the various lipid parameters. The results showed a significant increase (p <0.05) in serum high density lipoprotein level, and a decrease in serum low density lipoprotein level and cardiovascular risk indices (atherogenic index of plasma, castelli's risk index-I, castelli's risk index-II and atherogenic coefficient) in the treatment groups, with the maximum effect attained after 6 weeks of treatment. Also, photomicrographs of histologically examined cardiac muscle of the treatment groups appeared indifferent from that of the negative control. These findings may suggest that treatment with Revive capsule at the appropriate dosage for 6 weeks did not pose any cardiovascular risk or cardiotoxicty, but may rather be helpful in the amelioration of cardiovascular diseases in a rat model. [ABSTRACT FROM AUTHOR]

Heparan sulfate proteoglycans (HSPGs) are an important constituent of the macrophage glycocalyx and extracellular microenvironment. To examine their role in atherogenesis, we inactivated the biosynthetic gene N-acetylglucosamine N-deacetylase-N-sulfotransferase 1 (Ndst1) in macrophages and crossbred the strain to Ldlr(-/-) mice. When placed on an atherogenic diet, Ldlr(-/-)Ndst1(f/f)LysMCre(+) mice had increased atherosclerotic plaque area and volume compared to Ldlr(-/-) mice. Diminished sulfation of heparan sulfate resulted in enhanced chemokine expression; increased macrophages in plaques; increased expression of ACAT2, a key enzyme in cholesterol ester storage; and increased foam cell conversion. Motif analysis of promoters of upregulated genes suggested increased type I interferon signaling, which was confirmed by elevation of STAT1 phosphorylation induced by IFN-β. The proinflammatory macrophages derived from Ndst1(f/f)LysMCre(+) mice also sensitized the animals to diet-induced obesity. We propose that macrophage HSPGs control basal activation of macrophages by maintaining type I interferon reception in a quiescent state through sequestration of IFN-β.

Objective(s): Bisphenol A (BPA) that is a monomer of plastic products may possibly interfere with epigenetics and be involved in onset and progression of several diseases. This study was aimed to detect the epigenetic effects of in utero BPA exposure in mice offspring.Materials and Methods: All experiments were performed according to the national guidelines for laboratory animals and after ethical approval. Thirty adult BALB/c female mice were divided into 3 equal groups, G1 (controls), G2 (ethanol 0.10 ml/100ml of PBS so that final concentration would be 0.01%) vehicle control and G3 (BPA 10 mg/kg). Chemicals were given twice a week throughout the pregnancy. Once delivered at term, female offspring were observed for body weight, behavior and movements. Blood glucose, serum insulin, cholesterol and high-density lipoprotein cholesterol (HDLc) were measured at 5 and 15 months postnatal. Animals were sacrificed at 15 months and pancreas, kidney, adipose tissue and uterine tissue were taken and stained with either Hematoxylin and eosin (H & E) or immunostaining and examined under light microscope.Results: Offspring of group G3 revealed abnormal changes of body weight, behavior and movements. Blood glucose, serum insulin, cholesterol and HDLc were high in group G3 offspring compared to controls. H & E staining showed changes in the parenchyma of pancreas, kidneys and uterus, which were confirmed by staining with anti- islet-1, kidney-specific (Ksp) cadherin, and anti- MLH antibody. Conclusion: In utero exposure of BPA exerts diabetogenic and atherogenic effects with less parenchymal tissue in endocrine pancreas, kidney and uterus.

The present study compared the fatty acid profile and some physical parameters of eggs from hens reared according to the organic system at the beginning of the first and second laying cycle. A total of 1080 eggs were analysed at the beginning of the first (from the 28th to 30th week of age) and the second (from the 78th to 80th week of age) laying cycle. It was found that the hen ages influenced the egg weight, egg surface area, yolk proportion, and eggshell colour. Albumen and eggshell proportion, albumen, yolk index, Haugh unit score, and eggshell strength were lower in eggs from older hens compared with those produced from younger layers. Monounsaturated fatty acids were found in higher amounts than saturated fatty acids and polyunsaturated fatty acids in egg yolks of eggs from layers only at the beginning of the second laying cycle. The PUFAn-6/n-3 ratio, saturation, atherogenic, and thrombogenic indices were significantly lower in the egg yolks from older hens compared to younger layers. These findings (regarding the eggs from the older ones) prove that it is practical to utilize them in the organic farming system during a period of two years.

Objective: To evaluate the pattern of dyslipidaemia, risk factors, and comorbidities in young Indian adults with dyslipidaemia. Methods: A retrospective, multi-centric real-world study included individuals with dyslipidaemia, aged 18 - 45 years, attending to 623 hospitals/clinics across India. Data were collected retrospectively from medical records to note demographics, risk factors (smoking, alcohol consumption, sedentary lifestyle, family history of dyslipidaemia, diabetes mellitus, and hypertension), and clinical details (height, weight, waist circumference, body mass index (BMI), blood pressure, blood sugar, glycated hemoglobin (HbA1c), triglycerides (TG), total cholesterol (TC), low-density lipoproteins (LDL-C), and high-density lipoprotein (HDL-C)).A descriptive analysis and comparative analysis (Mann-Whitney U test and Chi-square test) were done. Results: Of the total 8135 patients, the majority were men (65.0%). Overall, 87.1% of population had one or multiple comorbidities which included the presence of dyslipidaemia alone (12.9%), dyslipidaemia with diabetes and hypertension (39.1%), dyslipidaemia with diabetes (33.6%), and dyslipidaemia with hypertension (14.4%). Sedentary lifestyle was prevalent observation in >50% of the population. Youngest age (18 - 25) group had higher prevalence of hypertriglyceridemia (63.2%), high LDL-C levels (56.8%), and low HDL-C levels (64.6%), while patients from the age group >25 to ≤35 years had the highest incidence of hypercholesterolemia (66.6%). Atherogenic dyslipidaemia was observed in 41.9%, 25.5%, and 23.2% of patients from age groups of ≥18 to ≤25, >25 to ≤35, and >35 to ≤45 years, respectively. Patients with HbA1c ≥6.5% had significantly higher levels of TG, TC, LDL-C, and lower HDL-C compared to those with HbA1c <6.5%. Conclusion: Hypertriglyceridemia, high LDL-C, low HDL-C, and atherogenic dyslipidaemia were prevalent in the young Indian cohort and sedentary lifestyle, and HbA1c ≥ 6.5% were the predominant risk factors of dyslipidaemia. [ABSTRACT FROM AUTHOR]

Copyright of Consensus (16803817) is the property of Universidad Femenina del Sagrado Corazon and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Coronary artery disease and ischemic stroke represent the first cause of mortality in Mexico. Epidemiological data suggest that the most common lipid abnormalities are low HDL-C levels and hypertriglyceridemia both related to an increase in BMI. The Mexican Society of Cardiology organized an expert panel to manifest our own guidelines in the diagnosis, evaluation and treatment of dyslipidemias and atherosclerosis. [ABSTRACT FROM AUTHOR]

Metabolically unhealthy overweight (MUO) individuals and metabolically healthy overweight (MHO) individuals differ in biomarkers of atherogenesis. Metabolomic approaches enable studies of the metabolic variables underlying these differences. We determined the metabolomes in plasma samples from 34 MUO and 34 MHO individuals matched for sex, age, and body mass index (BMI) to identify potential metabolic markers or pathways associated with atherogenic traits. This analysis revealed that the MUO group had significantly higher levels of glycolic acid, 6 lysophosphatidylethanolamines (lysoPEs), and 12 lysophosphatidylcholines (lysoPCs). Although the two groups had similar total body fat percentages and lean body masses, MUO individuals had larger visceral fat areas (VFAs). They also had greater circulating lipoprotein-associated phospholipase A 2 (Lp-PLA 2) activity and higher levels of oxidized low-density lipoprotein (ox-LDL) and urinary 8-epi-prostaglandin F 2α (8-epi-PGF 2α), reflecting higher risks for oxidative and lipid-related tissue damage. The following measures were positively correlated: VFA and ox-LDL; ox-LDL and Lp-PLA 2 activity; and lysoPC, lysoPE, and 8-epi-PGF 2α levels. Chronic plasma lysoPC increases were associated with atherogenic traits, higher levels of mean ox-LDL, 8-epi-PGF 2α , Lp-PLA 2 , and visceral fat accumulation in MUO compared to MHO individuals. This panel of plasma metabolites distinguishes MUO from MHO individuals and will enable future research on fat dysregulation and obesity. [ABSTRACT FROM AUTHOR]

Although mast cell functions have classically been related to allergic responses, recent studies indicate that these cells contribute to other common diseases such as multiple sclerosis, rheumatoid arthritis, atherosclerosis, aortic aneurysm and cancer. This study presents evidence that mast cells also contribute to diet-induced obesity and diabetes. For example, white adipose tissue (WAT) from obese humans and mice contain more mast cells than WAT from their lean counterparts. Furthermore, in the context of mice on a Western diet, genetically induced deficiency of mast cells, or their pharmacological stabilization, reduces body weight gain and levels of inflammatory cytokines, chemokines and proteases in serum and WAT, in concert with improved glucose homeostasis and energy expenditure. Mechanistic studies reveal that mast cells contribute to WAT and muscle angiogenesis and associated cell apoptosis and cathepsin activity. Adoptive transfer experiments of cytokine-deficient mast cells show that these cells, by producing interleukin-6 (IL-6) and interferon-gamma (IFN-gamma), contribute to mouse adipose tissue cysteine protease cathepsin expression, apoptosis and angiogenesis, thereby promoting diet-induced obesity and glucose intolerance. Our results showing reduced obesity and diabetes in mice treated with clinically available mast cell-stabilizing agents suggest the potential of developing new therapies for these common human metabolic disorders.

ObjectiveWestern-type high-fat/high-cholesterol diets used to induce atherogenesis in low-density lipoprotein (LDL) receptor-deficient mice also lead to obesity with concomitant metabolic complications, eg, hypertriglyceridemia, hyperinsulinemia, and insulin resistance. Our aim was to design a diet inducing atherosclerosis through moderate hypercholesterolemia without associated parameters of the metabolic syndrome.Methods and resultsMale LDL receptor-deficient mice were fed regular chow (RC; 0.01% cholesterol/4.4% fat), cholesterol-enriched regular chow (HC; 1% cholesterol/4.4% fat), or Western diet (WD 0.06% cholesterol/21% milk fat) for 28 weeks. HC-feeding led to elevated plasma (approximately 20.7 mmol/L [800 mg/dL]) and LDL cholesterol and accelerated atherosclerosis. Plasma triglycerides were unaffected. Compared with RC-fed controls, HC-fed mice had normal body weight gain and normal fasting levels of glucose, free fatty acids, and insulin. In contrast, WD-fed mice were extremely hypercholesterolemic (>41.4 mmol/L), obese, hypertriglyceridemic, hyperinsulinemic, insulin resistant, and showed adverse health such as skin/fur abnormalities and hepatic steatosis. Although atherosclerotic surface areas in the entire aorta were similar in HC-fed and WD-fed mice, lesions in aortic origin cross sections were significantly larger in WD-fed mice. However, morphology was similar in lesions of equal size.ConclusionsThe HC diet induced moderate hypercholesterolemia and extensive atherosclerosis and should be useful to study specific aspects of atherogenesis in the absence of confounding effects of the metabolic syndrome.

During the progression of atherosclerosis, autoantibodies are induced to epitopes of oxidized low-density lipoprotein (oxLDL) and active immunization of hypercholesterolemic mice with oxLDL ameliorates atherogenesis. We unexpectedly found that many autoantibodies to oxLDL derived from 'naive' atherosclerotic mice share complete genetic and structural identity with antibodies from the classic anti-phosphorylcholine B-cell clone, T15, which protect against common infectious pathogens, including pneumococci. To investigate whether in vivo exposure to pneumococci can affect atherogenesis, we immunized Ldlr(-/-) mice with Streptococcus pneumoniae. This induced high circulating levels of oxLDL-specific IgM and a persistent expansion of oxLDL-specific T15 IgM-secreting B cells primarily in the spleen, which were cross-reactive with pneumococcal determinants. Pneumococcal immunization decreased the extent of atherosclerosis, and plasma from these mice had an enhanced capacity to block the binding of oxLDL to macrophages. These studies show molecular mimicry between epitopes of oxLDL and S. pneumoniae and indicate that these immune responses can have beneficial effects.

Many patients with cardiovascular disease have their low density lipoprotein cholesterol within normal range. This raises the question about the most important lipoprotein to use as a marker of atherogenecity. In fact, small dense low density lipoprotein has recently been suggested as a strong predictor of cardiovascular disease. Among high risk patients, those with metabolic syndrome represent an important target population. Different methods of small dense low density lipoprotein measurement were developed. Accordingly, two phenotypes of low density lipoprotein are recognized: Phenotype A (predominance of large buoyant low density lipoprotein) & phenotype B (predominance of small dense low density lipoprotein). However, none of the methods has been yet considered as a gold standard one. A lot of studies confirmed the role of small dense low density lipoprotein in the development of cardiovascular disease through atherogenic properties & clinical trials. However, others failed to do so. These discrepancies may be due to different sample sizes, different populations, different age groups, different methods of measurement & other possible confounding factors. The aim of this review is to discuss the role of small dense low density lipoprotein as a valuable screening/preventive tool of cardiovascular disease in patients with metabolic syndrome.

Maternal hypercholesterolemia during pregnancy is associated with a marked increase in aortic fatty streak formation in human fetuses and faster progression of atherosclerosis during normocholesterolemic childhood. However, the mechanisms responsible are unknown, and the contribution of genetic differences is difficult to assess in humans. The goal of this study was to determine whether maternal hypercholesterolemia per se may cause enhanced fatty streak formation in offspring and whether interventions during pregnancy can reduce it. During pregnancy, 1 group of New Zealand White rabbits was fed control chow and 8 groups were fed hypercholesterolemic diets Chol 1 (yielding plasma cholesterol of 153 mg/dL) or Chol 2 (yielding 359 mg/dL) without or with cholestyramine, vitamin E, or both. Offspring (n=15 to 25 per group) were killed at birth. Maternal hypercholesterolemia enhanced mean lesion size in the aorta of their offspring at birth from 44+/-18x10(3) micrometer(2) per section in controls to 85+/-26x10(3) in Chol 1 and 156+/-49x10(3) in Chol 2 groups (P

To determine whether labeled antibodies against oxidized LDL (OxLDL) offer advantages for quantifying atherosclerosis, we compared in vivo aortic uptake of (125)I-labeled MDA2, a monoclonal antibody against malondialdehyde-lysine epitopes), atherosclerotic surface area, and aortic weight in Watanabe heritable hyperlipidemic and New Zealand White rabbits and in low density lipoprotein receptor-deficient (LDLR(-/-)) and apolipoprotein E-deficient (apoE(-/-)) mice. Absolute and specific uptakes of (125)I-MDA2 were significantly greater in plaque than in normal aortas. Uptake of (125)I-MDA2 significantly correlated with aortic weight and percent atherosclerotic surface area in rabbits and mice. To assess whether (125)I-MDA2 uptake reflects changes in lesion content of OxLDL, in a separate study, extensive atherosclerosis was induced in 4 groups of LDLR(-/-) mice by feeding them a high fat/cholesterol diet for 6 months. A baseline group was euthanized at this time. The remaining groups were fed "regression" diets (chow or chow+1% vitamin E+0.05% vitamin C) or the high fat/cholesterol diet for 6 more months. When atherosclerosis was measured as percent surface area or aortic weight, there was strong progression in the high fat/cholesterol group, moderate progression in the chow group, and no progression in the chow+vitamin E+vitamin C group compared with the baseline group. The (125)I-MDA2 method also yielded a significant increase in atherosclerosis in the high fat/cholesterol group but significant decreases in the chow and chow+vitamin E+vitamin C groups. Immunocytochemistry showed fewer oxidation-specific epitopes in lesions from the chow and chow+vitamin E+vitamin C groups. Thus, the uptake of (125)I-MDA2 correlates well with traditional measures of atherosclerosis but also reflects reduced plaque OxLDL content after hypocholesterolemic intervention.

Objective(s): Bisphenol A (BPA) that is a monomer of plastic products may possibly interfere with epigenetics and be involved in onset and progression of several diseases. This study was aimed to detect the epigenetic effects of in utero BPA exposure in mice offspring. Materials and Methods: All experiments were performed according to the national guidelines for laboratory animals and after ethical approval. Thirty adult BALB/c female mice were divided into 3 equal groups, G1 (controls), G2 (ethanol 0.10 ml/100ml of PBS so that final concentration would be 0.01%) vehicle control and G3 (BPA 10 mg/kg). Chemicals were given twice a week throughout the pregnancy. Once delivered at term, female offspring were observed for body weight, behavior and movements. Blood glucose, serum insulin, cholesterol and high-density lipoprotein cholesterol (HDLc) were measured at 5 and 15 months postnatal. Animals were sacrificed at 15 months and pancreas, kidney, adipose tissue and uterine tissue were taken and stained with either Hematoxylin and eosin (H & E) or immunostaining and examined under light microscope. Results: Offspring of group G3 revealed abnormal changes of body weight, behavior and movements. Blood glucose, serum insulin, cholesterol and HDLc were high in group G3 offspring compared to controls. H & E staining showed changes in the parenchyma of pancreas, kidneys and uterus, which were confirmed by staining with anti-islet-1, kidney-specific (Ksp) cadherin, and anti-MLH antibody. Conclusion: In utero exposure of BPA exerts diabetogenic and atherogenic effects with less parenchymal tissue in endocrine pancreas, kidney and uterus. [ABSTRACT FROM AUTHOR]

Elevated lipoprotein(a) (Lp[a]) is an independent, genetic risk factor for atherosclerotic cardiovascular disease (ASCVD) that impacts ~1.4 billion people globally. Generally, Lp(a) levels remain stable over time; thus, most individuals need only undergo Lp(a) testing through a non-fasting blood draw once in their lifetime, unless elevated Lp(a) is identified. Despite the convenience of the test for clinicians and patients, routine Lp(a) testing has not been widely adopted. This review provides a guide to the benefits of Lp(a) testing and solutions for overcoming common barriers in practice, including access to testing and lack of awareness. Lp(a) testing provides the opportunity to reclassify ASCVD risk and drive intensive cardiovascular risk factor management in individuals with elevated Lp(a), and to identify patients potentially less likely to respond to statins. Moreover, cascade screening can help to identify elevated Lp(a) in relatives of individuals with a personal or family history of premature ASCVD. Overall, given the profound impact of elevated Lp(a) on cardiovascular risk, Lp(a) testing should be an essential component of risk assessment by primary and specialty care providers., Competing Interests: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Ciffone – Previous consulting: Novartis. McNeal – Previous consulting: Novartis. McGowan – Previous participation in a Novartis advisory board. Ferdinand – Consulting: Amgen, Janssen, Medtronic, and Novartis., (© 2023 The Authors.)

Cardiovascular disease is prevalent globally and is the most common complication of metabolic syndrome (MetS). Previous studies have suggested that curcumin and probiotics may improve the lipid profile, so we aimed to investigate the effects of the edible powder enriched with these substances on lipid profile level and atherogenic indices such as Atherogenic Coefficient (AC), Castelli Risk Index-I (CRI-I), Castelli Risk Index-II (CRI-II), and Atherogenic Index of Plasma (AIP). In the present parallel randomized double-blinded placebo-controlled clinical trial, 124 people with MetS with overweight or obesity were randomly allocated to 4 groups and were followed up for 8 weeks. The participants received a low-calorie diet and a daily sachet of enriched powder drink. The sachets contained either 10 9  CFU of probiotics or 1 g of curcumin, or probiotic + curcumin (pro + cur), or placebo, respectively. The fasting lipid profile and atherogenic indices were measured at the beginning and end of the study. One hundred and fourteen participants completed the study. At the end of the study, the within- and between-group comparisons showed no significant differences in lipid profile and atherogenic indices ( p  > .05). Based on the results of the current study, taking an oral powder containing 1 g curcumin and 10 9  CFU probiotics for 8 weeks had no effect on the lipid profile level and atherogenic indices; however, more studies are recommended., Competing Interests: The authors declare no conflict of interest., (© 2023 The Authors. Food Science & Nutrition published by Wiley Periodicals LLC.)

The cis(c)-9, trans(t)-11 (c9,t11) and t10,c12 isomers of conjugated linoleic acid (CLA) have been reported as agonists of peroxisome proliferator-activated receptor (PPAR) and beneficial in lipidemia and glycemia. However, it is unclear whether CLA isomers enhance or antagonize effects of conventional drugs targeting PPAR. Male Sprague-Dawley rats were fed high fat diet (HFD) for 8 weeks and treated without or with CLA, rosiglitazone or both for 4 weeks. Oral glucose tolerance and surrogate markers of insulin resistance were not significantly different for all treatments compared to untreated normal diet (ND) or HFD group, except lipoprotein levels. The combination of CLA and rosiglitazone had suppressed levels of low and high density lipoproteins (46% and 25%, respectively), compared to HFD-alone. Conversely, the atherogenic co-efficient of the animals received HFD or HFD+rosiglitazone+CLA was 2-folds higher than ND, HFD+rosiglitazone or HFD+CLA. Isolated aortic rings from the combined CLA and rosiglitazone treated animals were less sensitive to isoprenaline-induced relaxation among endothelium-denuded aortas with a decreased efficacy and potency (Rmax=53±4.7%; pEC50=6±0.2) compared to endothelium-intact aortas (Rmax=100±9.9%; pEC50=7±0.2). Our findings illustrate that the combination of CLA and rosiglitazone precede the atherogenic state with impaired endotheliumindependent vasodilatation before the onset of HFD-induced insulin resistance. [ABSTRACT FROM AUTHOR]

In this study, the antihyperglycemic and antihyperlipidemic effects of Mangifera indica L. (MIL) young leaves extract were investigated using diabetic mice models. Male Mus musculus L. mice were intratoripeneally injected by Alloxan monohydrate (AM) to induce diabetes and were observed for 28 days. The blood glucose, total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL_C), low-density lipoprotein cholesterol (LD_LC) and atherogenic index were evaluated. The acute toxicity of MIL was determined at the dose of 1000, 2500, 5000 mg/kg body weight of normal mice. Diabetic mice were orally administrated with extract of MIL (150, 300, 450 mg/kg body weight/ twice a day). The results showed that the MIL significantly decreased the plasma glucose, TC, TG, LDL_C levels and atherogenic index and greatly elevated the HDL_C level in diabetic mice (p < 0.05). The methanol extract of young leaves showed the antidiabetic and antihyperlipidemic potential. Altogether, Mangiferine indica L. leaves could be considering as a promising therapy in preventing the complications of diabetes. [ABSTRACT FROM AUTHOR]

Many patients with cardiovascular disease have their low density lipoprotein cholesterol within normal range. This raises the question about the most important lipoprotein to use as a marker of atherogenecity. In fact, small dense low density lipoprotein has recently been suggested as a strong predictor of cardiovascular disease. Among high risk patients, those with metabolic syndrome represent an important target population. Different methods of small dense low density lipoprotein measurement were developed. Accordingly, two phenotypes of low density lipoprotein are recognized: Phenotype A (predominance of large buoyant low density lipoprotein) & phenotype B (predominance of small dense low density lipoprotein). However, none of the methods has been yet considered as a gold standard one. A lot of studies confirmed the role of small dense low density lipoprotein in the development of cardiovascular disease through atherogenic properties & clinical trials. However, others failed to do so. These discrepancies may be due to different sample sizes, different populations, different age groups, different methods of measurement & other possible confounding factors. The aim of this review is to discuss the role of small dense low density lipoprotein as a valuable screening/preventive tool of cardiovascular disease in patients with metabolic syndrome. [ABSTRACT FROM AUTHOR]

Background & Aims NOD-like receptor protein 3 (NLRP3) inflammasome activation occurs in Non-alcoholic fatty liver disease (NAFLD). We used the first small molecule NLRP3 inhibitor, MCC950, to test whether inflammasome blockade alters inflammatory recruitment and liver fibrosis in two murine models of steatohepatitis. Methods We fed foz/foz and wild-type mice an atherogenic diet for 16 weeks, gavaged MCC950 or vehicle until 24 weeks, then determined NAFLD phenotype. In mice fed an methionine/choline deficient (MCD) diet, we gavaged MCC950 or vehicle for 6 weeks and determined the effects on liver fibrosis. Results In vehicle-treated foz/foz mice, hepatic expression of NLRP3, pro-IL-1β, active caspase-1 and IL-1β increased at 24 weeks, in association with cholesterol crystal formation and NASH pathology; plasma IL-1β, IL-6, MCP-1, ALT/AST all increased. MCC950 treatment normalized hepatic caspase 1 and IL-1β expression, plasma IL-1β, MCP-1 and IL-6, lowered ALT/AST, and reduced the severity of liver inflammation including designation as NASH pathology, and liver fibrosis. In vitro, cholesterol crystals activated Kupffer cells and macrophages to release IL-1β; MCC950 abolished this, and the associated neutrophil migration. MCD diet-fed mice developed fibrotic steatohepatitis; MCC950 suppressed the increase in hepatic caspase 1 and IL-1β, lowered numbers of macrophages and neutrophils in the liver, and improved liver fibrosis. Conclusion MCC950, an NLRP3 selective inhibitor, improved NAFLD pathology and fibrosis in obese diabetic mice. This is potentially attributable to the blockade of cholesterol crystal-mediated NLRP3 activation in myeloid cells. MCC950 reduced liver fibrosis in MCD-fed mice. Targeting NLRP3 is a logical direction in pharmacotherapy of NASH. Lay summary Fatty liver disease caused by being overweight with diabetes and a high risk of heart attack, termed non-alcoholic steatohepatitis (NASH), is the most common serious liver disease with no current treatment. There could be several causes of inflammation in NASH, but activation of a protein scaffold within cells termed the inflammasome (NLRP3) has been suggested to play a role. Here we show that cholesterol crystals could be one pathway to activate the inflammasome in NASH. We used a drug called MCC950, which has already been shown to block NLRP3 activation, in an attempt to reduce liver injury in NASH. This drug partly reversed liver inflammation, particularly in obese diabetic mice that most closely resembles the human context of NASH. In addition, such dampening of liver inflammation in NASH achieved with MCC950 partly reversed liver scarring, the process that links NASH to the development of cirrhosis. [ABSTRACT FROM AUTHOR]

Background: Broiler meat is an essential source of food due to its favourable effects on human health derived from its protein, fats, minerals, vitamins and its bioactive components. Methods: A total of 90 carcasses were collected from the retail market in Jeddah city, Saudi Arabia during April, May and June 2014 to determine the effects of meat type (frozen vs. fresh) and sources within fresh types (A, B, C) vs. frozen types (D, E and F) on their fatty acid profiles, cholesterol, their hypocholesterolemic, atherogenic and thrombogenic indices, and on their antioxidants' status. Results: The sources of meat had a significant effect on the hypocholesterolemic and atherogenic indices, with the D source of fresh meat having the best indices. Total saturated fatty acids (SFA), unsaturated fatty acids (UFA), the UFA/SAF ratio, and the monounsaturated (MUFA), Omega-6 and Omega-7 fatty acids were significantly affected by the source of meat. The results revealed that the D source of fresh meat showed favourable fatty acid profiles with significant health benefits for human. Correlation analyses showed a significant negative relationship between the SFA and hypocholesterolemic indices, and significant positive relationships with the atherogenic index, the thrombotgenic index and the total antioxidant capacity. In addition, the relationship between UFA and the hypocholesterolemic index was strongly significantly positive, but was highly negative between the atherogenic and thrombotic indices. The correlations between omega-6 and total cholesterol and the atherogenic index was moderately negative, but was moderately positive with the hypocholesterolemic index. Conclusion: Fatty acids profiles and the hypocholesterolemic and atherogenic indices of broiler meat in the retail market in Jeddah city, Saudi Arabia during April-May-June showed significant differences, with the potential for favourable fatty acids to be boosted. Such variability indicates the needs for a feeding strategy to enhance the favourable fatty acids that may positively impact the health of the consumer, lowering the risk of hypercholesterolemia, atherosclerosis, and thrombogenesis although further studies are needed. [ABSTRACT FROM AUTHOR]

Introduction: Atherosclerosis is a progressive disease that develops in areas of disturbed flow (d-flow). Progressive atherosclerosis is characterized by bulky plaques rich in mesenchymal cells and high-grade inflammation that can rupture leading to sudden cardiac death or acute myocardial infarction. In response to d-flow, endothelial cells acquire a mesenchymal phenotype through endothelial-to-mesenchymal transition (EndMT). However, the signaling intermediaries that link d-flow to EndMT are incompletely understood., Methods and Results: In this study we found that in human atherosclerosis, cells expressing SNAI1 (Snail 1, EndMT transcription factor) were highly expressed within the endothelial cell (EC) layer and in the pre-necrotic areas in unstable lesions, whereas stable lesions did not show any SNAI1 positive cells, suggesting a role for EndMT in lesion instability. The interleukin-1 (IL-1), which signals through the type-I IL-1 receptor (IL-1R1), has been implicated in plaque instability and linked to EndMT formation in vitro . Interestingly, we observed an association between SNAI1 and IL-1R1 within ECs in the unstable lesions. To establish the causal relationship between EndMT and IL-1R1 expression, we next examined IL-1R1 levels in our Cre-lox endothelial-specific lineage tracing mice. IL-1R1 and Snail1 were highly expressed in ECs under atheroprone compared to athero-protective areas, and oscillatory shear stress (OSS) increased IL-1R1 protein and mRNA levels in vitro . Exposure of ECs to OSS resulted in loss of their EC markers and higher induction of EndMT markers. By contrast, genetic silencing of IL-1R1 significantly reduced the expression of EndMT markers and Snail1 nuclear translocation, suggesting a direct role for IL-1R1 in d-flow-induced EndMT. In vivo , re-analysis of scRNA-seq datasets in carotid artery exposed to d-flow confirmed the IL-1R1 upregulation among EndMT population, and in our partial carotid ligation model of d-flow, endothelial cell specific IL-1R1 KO significantly reduced SNAI1 expression., Discussion: Global inhibition of IL-1 signaling in atherosclerosis as a therapeutic target has recently been tested in the completed CANTOS trial, with promising results. However, the data on IL-1R1 signaling in different vascular cell-types are inconsistent. Herein, we show endothelial IL-1R1 as a novel mechanosensitive receptor that couples d-flow to IL-1 signaling in EndMT., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2023 Kidder, Pea, Cheng, Koppada, Visvanathan, Henderson, Thuzar, Yu and Alfaidi.)

This analysis evaluates the effects on lipoprotein subfractions and LDL particle size of ezetimibe/simvastatin with or without coadministration of fenofibrate in patients with mixed hyperlipidemia. This multicenter, double-blind, placebo-controlled, parallel-group study included 611 patients aged 18–79 years randomized in 1:3:3:3 ratios to one of four 12 week treatment groups: placebo; ezetimibe/simvastatin 10/20 mg/day; fenofibrate 160 mg/day; or ezetimibe/simvastatin 10/20 mg/day + fenofibrate 160 mg/day. At baseline and study endpoint, cholesterol associated with VLDL, intermediate density lipoprotein (IDL), LDL, and HDL subfractions was quantified using the Vertical Auto Profile II method. LDL particle size was determined using segmented gradient gel electrophoresis. Whereas fenofibrate reduced cholesterol mass within VLDL and IDL, and shifted cholesterol from dense LDL subfractions into the more buoyant subfractions and HDL, ezetimibe/simvastatin reduced cholesterol mass within all apolipoprotein B-containing particles without significantly shifting the LDL particle distribution profile. When administered in combination, the effects of the drugs were complementary, with more-pronounced reductions in VLDL, IDL, and LDL, preferential loss of more-dense LDL subfractions, and increased HDL, although the effects on most lipoprotein subfractions were not additive. Thus, ezetimibe/simvastatin + fenofibrate produced favorable effects on atherogenic lipoprotein subclasses in patients with mixed hyperlipidemia.

Alcohol is metabolized by alcohol-dehydrogenase into acetaldehyde, and by aldehyde-dehydrogenase and acetyl-coenzyme-A into acetate. Thus produced hydrogen is accepted by nicotinamide-adenine-dinucleotide, which leads to the accumulation of fatty acids in the liver. Cirrhosis of the liver develops due to the intake of alcohol, 80g/day for men and 20g/day for women. The aim of this study was to determine the profile of plasma atherogenic factors in patients with alcoholic cirrhosis of the liver, compared to patients with HCV-cirrhosis, and to determinate their diagnostic significance. The study compared a total cholesterol (TC), triglycerides (Tg), high-density-lipoprotein-cholesterol (HDL-C), lowdensity- lipoprotein-cholesterol (LDL-C), and apoliproteins (ApoA1 and ApoB) in plasma of patients with alcoholic cirrhosis compared to patients with HCV-cirrhosis. The values of TC/HDL-C, ApoB/ApoA1 and LDL-C/HDL-C were calculated and compared in both groups. The study included 37 patients with alcoholic cirrhosis, mean age 52.65 years (SD-6.73), who consumed alcoholic beverages during an average of 8.67 years (SD-1.96) and 35 patients with HCV-cirrhosis. There were 21.62% of women and 78.38% of men with alcoholic cirrhosis, and 34.29% of women and 65.71% of men with HCV-cirrhosis. The average values for the following parameters in alcoholic cirrhosis were obtained: TG 11.91mmol/l (SD-2.51), TC 14.63 (SD-2.62), LDL-C - 8.77 mmol/l (SD-2.19), HDL-C 0.41 mmol/l (SD-0.09), apolipoprotein-B 4.01g/l (SD-0.18), apolipoprotein-A1 0.51g/l (SD-0.08); in HCV-cirrhosis, the average values of the studied parameters were as follows: TG 8,62mmol/l (SD-2.31), TC 9.67 (SD-2.39), LDL-C 6.12 mmol/l (SD-1.78), HDL-C 0.76 mmol/l (SD-0.09), apolipoprotein-B 2.38g/l (SD-0.16), apolipoprotein-A1 0.98g/l (SD-0.05). The apolipoprotein-B/apolipoprotein-A1 relation can serve as a diagnostic marker for the presence of alcoholic cirrhosis, and is a better indicator of atherogenic risk. [ABSTRACT FROM AUTHOR]

The homocysteine theory of arteriosclerosis received credence when it was shown that after a methionine load, circulating homocysteine-cysteine concentrations were higher in cardiovascular disease patients than in healthy controls. Subsequent studies showing associations between homocysteine and coronary artery disease, stroke and cognitive impairment, relied on small increases in homocysteine concentration unlike the very high homocysteine seen in the rare genetic disorders that lead to homocystinuria and much higher homocysteine levels. Subsequent studies in cell culture, animals, and humans showed that a variety of cardiovascular adverse effects of "high homocysteine" introduced either as a nonphysiological bolus or as a methionine load led to high homocysteine. We fed apolipoprotein E-deficient mice diets designed to achieve three conditions: (1) high methionine intake with normal blood homocysteine, (2) highmethionine intake with B vitamin deficiency and hyperhomocysteinemia, and (3) normalmethionine intake with both B vitamin deficiency and hyperhomocysteinemia.We found that the mice fed methionine-rich diets had significant atheromatous pathology in the aortic arch even with normal plasma homocysteine levels. Mice fed B vitamin-deficient diets developed severe hyperhomocysteinemia but without any increase in vascular pathology. Our findings suggest that even moderate increases in methionine intake are atherogenic in susceptible mice while high plasma homocysteine is not. [ABSTRACT FROM AUTHOR]