Familial hypercholesterolemia (FH) is a relatively rare genetic disease associated with high serum cholesterol levels but also with abnormalities in blood coagulation. Novel pharmacotherapeutic approaches in FH including proprotein convertase subtilisin/kexin type 9 antibodies (PCSK9Ab) are very efficient in decreasing cholesterol levels but their impact on coagulation in FH is not yet established. Therefore, we hypothesized that these novel antidyslipidemic drugs can positively impact blood coagulation due to their more potent effect on cholesterol. A total of 15 healthy volunteers and all 15 available patients with severe FH treated at the University Hospital Hradec Králové were enrolled, coagulation was assessed by mechanic coagulometer, and the impact of four clinically used direct anticoagulants was analyzed ex vivo. FH patients were treated effectively as their total cholesterol was 4.11 ± 1.57 mM and LDL cholesterol was 2.44 ± 1.46 mM, which were even lower values than detected in our generally healthy controls. Twelve from the 15 FH patients were finally analyzed as 3 were treated with anticoagulants. Coagulation in FH patients was prolonged more extensively by dabigatran and rivaroxaban, when compared to healthy controls. Treatment with PCSK9Ab or lipid apheresis did not seem to have a significant effect on coagulation. The latter procedure however significantly decreased serum levels of one vitamin K form, MK4. Shorter coagulation time was associated with higher levels of LDL, non-HDL, and total cholesterol. Current treatment of FH seems to improve the effects of direct anticoagulants beyond known effects on LDL cholesterol levels.

• Keywords
• Direct anticoagulants, Familial hypercholesterolemia, Proprotein convertase subtilisin/kexin type 9, Vitamin K,
• MeSH
• Anticholesteremic Agents therapeutic use   MeSH
• Anticoagulants * therapeutic use   pharmacology   MeSH
• Cholesterol blood   MeSH
• Dabigatran therapeutic use   pharmacology   MeSH
• Adult MeSH
• Blood Coagulation * drug effects   MeSH
• Hyperlipoproteinemia Type II * blood   drug therapy   MeSH
• Hypolipidemic Agents * therapeutic use   pharmacology   MeSH
• Cholesterol, LDL blood   MeSH
• Middle Aged MeSH
• Humans MeSH
• PCSK9 Inhibitors MeSH
• Proprotein Convertase 9 MeSH
• Rivaroxaban therapeutic use   pharmacology   MeSH
• Case-Control Studies MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Anticholesteremic Agents MeSH
• Anticoagulants * MeSH
• Cholesterol MeSH
• Dabigatran MeSH
• Hypolipidemic Agents * MeSH
• Cholesterol, LDL MeSH
• PCSK9 Inhibitors MeSH
• PCSK9 protein, human MeSH Browser
• Proprotein Convertase 9 MeSH
• Rivaroxaban MeSH

INTRODUCTION: Early and lifelong treatment is essential in patients with familial hypercholesterolaemia (FH) due to genetically elevated low-density lipoprotein cholesterol (LDL-C) from the first years of life. In women with FH, lipid-lowering treatment is interrupted during childbearing years due to contraindication of the medication during conception, pregnancy and breastfeeding. However, little is known about the impact of breastfeeding on lipid profile and other risk markers for atherosclerotic cardiovascular disease (ASCVD) in women with FH compared with women without hypercholesterolaemia, and to what extent statins transfer into breast milk.We aim to investigate (1) the association between breastfeeding and serum lipid profile in women with and without FH; (2) the association between breastfeeding and other ASCVD risk markers in women with and without FH and (3) the concentration of statins in breast milk of women with FH. METHODS AND ANALYSIS: FH-FEMINA is a prospective study aiming to include 50 women with FH in Norway, the Netherlands and the Czech Republic. Additionally, 20 women without hypercholesterolaemia will be enrolled as a control group in Norway. Women will be included at the first study visit in gestational week 36, and follow-up visits will be scheduled at 2-4 weeks, and at 3, 6, 9 and 12 months postpartum. Information on lifestyle factors, treatment history and current and previous pregnancies will be collected. At each visit, a non-fasting blood sample, breast milk sample and information on diet, body mass index and blood pressure will be collected. Additional blood samples will be collected from the women with FH at 2, 4, 5, 7, 8, 10 and 11 months postpartum for as long as they are breastfeeding. At (re-)initiation of statin treatment, breast milk samples from women with FH will be collected for drug concentration measurements. ETHICS AND DISSEMINATION: Ethical approval will be obtained prior to study start in all three countries. Participants will be informed about the study and receive ample time to ask questions before the informed consent form is signed. The findings from this study will be disseminated to healthcare professionals, researchers and patients via peer-reviewed scientific article(s), conferences, patient organisations and social media. TRIAL REGISTRATION NUMBER: NCT05367310.

• Keywords
• Cardiovascular Disease, Coronary heart disease, Maternal medicine, Postpartum Women, Primary Prevention,
• MeSH
• Biomarkers blood   MeSH
• Adult MeSH
• Hyperlipoproteinemia Type II * blood   drug therapy   complications   MeSH
• Cardiovascular Diseases * MeSH
• Breast Feeding * MeSH
• Humans MeSH
• Lipids * blood   MeSH
• Milk, Human * chemistry   metabolism   MeSH
• Prospective Studies MeSH
• Heart Disease Risk Factors MeSH
• Hydroxymethylglutaryl-CoA Reductase Inhibitors * therapeutic use   MeSH
• Check Tag
• Adult MeSH
• Humans MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Clinical Trial Protocol MeSH
• Geographicals
• Czech Republic MeSH
• Netherlands MeSH
• Norway MeSH
• Names of Substances
• Biomarkers MeSH
• Lipids * MeSH
• Hydroxymethylglutaryl-CoA Reductase Inhibitors * MeSH

BACKGROUND AND AIMS: Overweight and obesity are modifiable risk factors for atherosclerotic cardiovascular disease (ASCVD) in the general population, but their prevalence in individuals with heterozygous familial hypercholesterolaemia (HeFH) and whether they confer additional risk of ASCVD independent of LDL cholesterol (LDL-C) remains unclear. METHODS: Cross-sectional analysis was conducted in 35 540 patients with HeFH across 50 countries, in the EAS FH Studies Collaboration registry. Prevalence of World Health Organization-defined body mass index categories was investigated in adults (n = 29 265) and children/adolescents (n = 6275); and their association with prevalent ASCVD. RESULTS: Globally, 52% of adults and 27% of children with HeFH were overweight or obese, with the highest prevalence noted in Northern Africa/Western Asia. A higher overweight/obesity prevalence was found in non-high-income vs. high-income countries. Median age at familial hypercholesterolaemia diagnosis in adults with obesity was 9 years older than in normal weight adults. Obesity was associated with a more atherogenic lipid profile independent of lipid-lowering medication. Prevalence of coronary artery disease increased progressively across body mass index categories in both children and adults. Compared with normal weight, obesity was associated with higher odds of coronary artery disease in children (odds ratio 9.28, 95% confidence interval 1.77-48.77, adjusted for age, sex, lipids, and lipid-lowering medication) and coronary artery disease and stroke in adults (odds ratio 2.35, 95% confidence interval 2.10-2.63 and odds ratio 1.65, 95% confidence interval 1.27-2.14, respectively), but less consistently with peripheral artery disease. Adjusting for diabetes, hypertension and smoking modestly attenuated the associations. CONCLUSIONS: Overweight and obesity are common in patients with HeFH and contribute to ASCVD risk from childhood, independent of LDL-C and lipid-lowering medication. Sustained body weight management is needed to reduce the risk of ASCVD in HeFH.

• Keywords
• Adiposity, Atherosclerosis, Dyslipidaemia, Insulin resistance,
• MeSH
• Child MeSH
• Adult MeSH
• Heterozygote MeSH
• Hyperlipoproteinemia Type II * epidemiology   complications   genetics   MeSH
• Body Mass Index MeSH
• Cardiovascular Diseases * epidemiology   etiology   MeSH
• Cholesterol, LDL metabolism   MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Young Adult MeSH
• Overweight * epidemiology   complications   MeSH
• Obesity * epidemiology   complications   MeSH
• Prevalence MeSH
• Cross-Sectional Studies MeSH
• Registries MeSH
• Risk Factors MeSH
• Aged MeSH
• Check Tag
• Child MeSH
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Young Adult MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Multicenter Study MeSH
• Names of Substances
• Cholesterol, LDL MeSH

Constitutive androstane receptor (CAR) and pregnane X receptor (PXR) are closely related nuclear receptors with overlapping regulatory functions in xenobiotic clearance but distinct roles in endobiotic metabolism. Car activation has been demonstrated to ameliorate hypercholesterolemia by regulating cholesterol metabolism and bile acid elimination, whereas PXR activation is associated with hypercholesterolemia and liver steatosis. Here we show a human CAR agonist/PXR antagonist, MI-883, which effectively regulates genes related to xenobiotic metabolism and cholesterol/bile acid homeostasis by leveraging CAR and PXR interactions in gene regulation. Through comprehensive analyses utilizing lipidomics, bile acid metabolomics, and transcriptomics in humanized PXR-CAR-CYP3A4/3A7 mice fed high-fat and high-cholesterol diets, we demonstrate that MI-883 significantly reduces plasma cholesterol levels and enhances fecal bile acid excretion. This work paves the way for the development of ligands targeting multiple xenobiotic nuclear receptors. Such ligands hold the potential for precise modulation of liver metabolism, offering new therapeutic strategies for metabolic disorders.

• MeSH
• Cholesterol metabolism   blood   MeSH
• Cytochrome P-450 CYP3A genetics   metabolism   MeSH
• Diet, High-Fat adverse effects   MeSH
• Hypercholesterolemia * drug therapy   metabolism   etiology   MeSH
• Hypolipidemic Agents * pharmacology   therapeutic use   MeSH
• Liver metabolism   drug effects   MeSH
• Constitutive Androstane Receptor MeSH
• Humans MeSH
• Disease Models, Animal MeSH
• Mice, Inbred C57BL MeSH
• Mice MeSH
• Pregnane X Receptor * antagonists & inhibitors   metabolism   genetics   MeSH
• Receptors, Cytoplasmic and Nuclear * agonists   metabolism   genetics   antagonists & inhibitors   MeSH
• Bile Acids and Salts metabolism   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Male MeSH
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Cholesterol MeSH
• Cytochrome P-450 CYP3A MeSH
• Hypolipidemic Agents * MeSH
• Constitutive Androstane Receptor MeSH
• Pregnane X Receptor * MeSH
• Receptors, Cytoplasmic and Nuclear * MeSH
• Bile Acids and Salts MeSH

Metabolic syndrome (MetS) represents a worldwide health problem, affecting cardiovascular and mental health. People with MetS are often suffering from depression. We used hereditary hypertriacylglycerolemic (HTG) rats as an animal model of MetS, and these were fed a high-fat-high-fructose diet (HFFD) to imitate unhealthy eating habits of people having several MetS risk factors and suffering depression. Male HTG rats were fed a standard diet (HTG-SD) or HFFD for eight weeks (HFFD8). Venlafaxine was administered for the last three weeks of the experiment (HFFD8+VE). Heart function was observed on the level of intact organisms (standard ECG in vivo), isolated hearts (perfusion according to Langendorff ex vivo), and molecular level, using the RT-PCR technique. The function of the isolated perfused heart was monitored under baseline and ischemia/reperfusion conditions. Analysis of ECG showed electrical abnormalities in vivo, such as significant QRS complex prolongation and increased heart rate. Ex vivo venlafaxine significantly reduced QT interval after ischemia/reperfusion injury. Baseline values of contractile abilities of the heart tended to be suppressed by HFFD. A significant reduction of LVDP was present in the HFFD8 group. Molecular analysis of specific genes involved in cardiac electrical (Cacna1c, Scn5a), contractile (Myh6, Myh7), metabolic function (Pgc1alpha) and calcium handling (Serca2a, Ryr2) supported some of the functional findings in vivo and ex vivo. Based on the present effect of venlafaxine on heart function, further research is needed regarding its cardiometabolic safety in the treatment of patients with MetS suffering from depression. Keywords: Metabolic syndrome, Venlafaxine, ECG, Cardiac contraction, Ischemia/Reperfusion.

• MeSH
• Diet, High-Fat * adverse effects   MeSH
• Fructose * adverse effects   administration & dosage   MeSH
• Hypertriglyceridemia * genetics   complications   drug therapy   MeSH
• Cardiovascular Diseases * etiology   prevention & control   MeSH
• Rats MeSH
• Metabolic Syndrome * drug therapy   physiopathology   MeSH
• Rats, Wistar MeSH
• Venlafaxine Hydrochloride * pharmacology   therapeutic use   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Fructose * MeSH
• Venlafaxine Hydrochloride * MeSH

BACKGROUND: Familial dysbetalipoproteinemia (FD) is an autosomal recessive (rarely dominant) inherited disorder that is almost exclusively associated with the apolipoprotein E gene (APOE) variability. Nonetheless, only a small proportion of APOE2/E2 subjects develop the phenotype for mixed dyslipidemia; the context of other trigger metabolic or genetic factors remains unknown. METHODS: One hundred and one patients with FD and eighty controls (all APOE2/E2 homozygotes; rs429358) were screened for 18 single-nucleotide polymorphisms (SNPs) within the genes involved in triglyceride metabolism. RESULTS: Two SNPs were significantly associated with the FD phenotype (rs439401 within APOE; P < 0.0005 and rs964184 within ZPR1/APOA5/A4/C3/A1 gene cluster; P < 0.0001). Unweighted genetic risk scores - from these two SNPs (GRS2), and, also, additional 13 SNPs with P-value below 0.9 (GRS15) - were created as an additional tool to improve the risk estimation of FD development in subjects with the APOE2/E2 genotype. Both GRS2 and GRS15 were significantly (P < 0.0001) increased in patients and both GRSs discriminated almost identically between the groups (P = 0.86). Subjects with an unweighted GRS2 of three or more had an almost four-fold higher risk of FD development than other individuals (odds ratio (OR) 3.58, 95% confidence interva (CI): 1.78-7.18, P < 0.0005). CONCLUSIONS: We identified several SNPs that are individual additive factors influencing FD development. The use of unweighted GRS2 is a simple and clinically relevant tool that further improves the prediction of FD in APOE2/E2 homozygotes with corresponding biochemical characteristics.

• Keywords
• Cardiovascular risk, Familial dysbetalipoproteinemia, Genetic risk score, Polymorphism,
• MeSH
• Apolipoprotein E2 * genetics   MeSH
• Adult MeSH
• Genetic Risk Score MeSH
• Genotype MeSH
• Hyperlipoproteinemia Type III * genetics   MeSH
• Polymorphism, Single Nucleotide MeSH
• Middle Aged MeSH
• Humans MeSH
• Aged MeSH
• Case-Control Studies MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Apolipoprotein E2 * MeSH

BACKGROUND AND AIMS: It is well known that elevated cholesterol is associated with enhanced platelet aggregation and patients suffering from familial hypercholesterolemia (FH) have a high risk of thrombotic cardiovascular events. Although decreasing cholesterol level is associated with attenuation of platelet hyperactivity, there are currently no data on the effect of convertase subtilisin/kexin type 9 monoclonal antibodies (PCSK9ab) on platelet reactivity in FH. The aim of the study was to analyse the impact of different therapies including PCSK9ab on platelet aggregation in FH. METHODS: This study enrolled all 15 patients treated in the University Hospital Hradec Králové for FH. PCSK9ab have been administered in 12 of 15 patients while 8 patients were also undergoing lipid apheresis. Blood samples from all patients including pre- and post-apheresis period were tested for platelet aggregation triggered by 7 inducers, and the effect of 3 clinically used drugs (acetylsalicylic acid, ticagrelor and vorapaxar) was compared as well. RESULTS: Although apheresis decreased the reactivity of platelets in general, platelet responses were not different between non-apheresis patients treated with PCSK9ab and apheresis patients (post-apheresis values) with the exception of ristocetin. However, when compared to age-matched healthy population, FH patients had significantly lower platelet aggregation responses to 4 out of 7 used inducers and higher profit from 2 out of 3 used antiplatelet drugs even after exclusion of FH patients regularly receiving conventional antiplatelet treatment. CONCLUSION: This study showed for the first time the suitability of PCSK9ab treatment for reduction of platelet reactivity in FH patients.

• Keywords
• ADP receptor, Acetylsalicylic acid, Antiplatelet, Dyslipidemia, Ticagrelor, Vorapaxar,
• MeSH
• Platelet Aggregation * drug effects   MeSH
• Adult MeSH
• Hyperlipoproteinemia Type II * blood   therapy   drug therapy   MeSH
• Platelet Aggregation Inhibitors * therapeutic use   pharmacology   MeSH
• Middle Aged MeSH
• Humans MeSH
• Antibodies, Monoclonal therapeutic use   pharmacology   MeSH
• PCSK9 Inhibitors * MeSH
• Proprotein Convertase 9 * immunology   MeSH
• Aged MeSH
• Blood Component Removal * MeSH
• Blood Platelets drug effects   metabolism   immunology   MeSH
• Treatment Outcome MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Platelet Aggregation Inhibitors * MeSH
• Antibodies, Monoclonal MeSH
• PCSK9 Inhibitors * MeSH
• PCSK9 protein, human MeSH Browser
• Proprotein Convertase 9 * MeSH

BACKGROUND: The role of fatty acids (FA) in the pathogenesis of insulin resistance and hyperlipidemia is a subject of intensive research. Several recent works have suggested cis-vaccenic acid (cVA) in plasma lipid compartments, especially in plasma phospholipids (PL) or erythrocyte membranes, could be associated with markers of insulin sensitivity and cardiovascular health. Nevertheless, not all the results of research work testify to these beneficial effects of cVA. Therefore, we decided to investigate the relations of proportion of cVA in plasma PL to markers of insulin resistance in hyperlipidemic men. SUBJECTS: In 231 men (median age 50) with newly diagnosed hyperlipidemia, we analyzed basic clinical parameters together with FA composition of plasma PL and stratified them according to the content of cVA into upper quartile (Q4) and lower quartile (Q1) groups. We examined also small control group of 50 healthy men. RESULTS: The individuals in Q4 differed from Q1 by lower plasma insulin (p < 0.05), HOMA-IR values (p < 0.01), and apolipoprotein B concentrations (p < 0.001), but by the higher total level of nonesterified FA (p < 0.01). Both groups had similar age, anthropometrical, and other lipid parameters. In plasma PL, the Q4 group had lower content of the sum of n-6 polyunsaturated FA, due to decrease of γ-linolenic and dihomo-γ-linolenic acids, whereas the content of monounsaturated FA (mainly oleic and palmitoleic) was in Q4 higher. CONCLUSIONS: Our results support hypothesis that plasma PL cVA could be associated with insulin sensitivity in men with hyperlipidemia.

• MeSH
• Apolipoproteins B blood   MeSH
• Biomarkers * blood   MeSH
• Adult MeSH
• Phospholipids * blood   MeSH
• Hyperlipidemias * blood   MeSH
• Insulin blood   MeSH
• Insulin Resistance * MeSH
• Oleic Acids * blood   MeSH
• Middle Aged MeSH
• Humans MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Apolipoproteins B MeSH
• Biomarkers * MeSH
• cis-vaccenic acid MeSH Browser
• Phospholipids * MeSH
• Insulin MeSH
• Oleic Acids * MeSH

This study investigated the therapeutic potential of probiotic bifidobacteria, isolated from Iranian fermented dairy products, in a hyperlipidemic animal model. Bifidobacterium strains were extracted from traditional dairy samples and screened using physiological and phenotypic examinations, 16S rRNA analysis, and probiotic properties such as tolerance to gastrointestinal juice, antimicrobial activity, and antibiotic susceptibility. The ability of the screened bifidobacteria to reduce serum and liver lipids in vivo was tested using male Wistar rats. Six strains of bifidobacteria were isolated from traditional Iranian fermented dairy. These strains showed promising in vitro activity in lowering triglyceride and cholesterol, tolerance to simulated gastrointestinal juice, the ability to adhere to Caco-2 cells, acceptable antibiotic susceptibility, and a broad spectrum of antibacterial activity. The diet supplemented with isolated bifidobacteria significantly reduced serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), liver tissue lipid levels, and hepatic enzymes in animals when compared to a high-fat diet without strains (p < 0.01). Additionally, the potential probiotic-supplemented diet significantly increased bile acid excretion in the feces and upregulated hepatic CYP7A1 expression levels (p < 0.05), while NPC1L1, ACAT2, and MTP gene expressions in small intestinal cells were downregulated (p < 0.05). Bifidobacteria isolated from Iranian traditional dairy showed potential for use in the production of fermented foods that have hypolipemic activity in the host.

• Keywords
• Bifidobacteria, Cholesterol-lowering, Probiotics, Triglyceride-lowering,
• MeSH
• Anti-Bacterial Agents pharmacology   MeSH
• Bifidobacterium * genetics   isolation & purification   metabolism   MeSH
• Caco-2 Cells MeSH
• Cholesterol 7-alpha-Hydroxylase genetics   metabolism   MeSH
• Cholesterol blood   metabolism   MeSH
• Feces microbiology   MeSH
• Hyperlipidemias * MeSH
• Liver metabolism   MeSH
• Rats MeSH
• Humans MeSH
• Dairy Products microbiology   MeSH
• Disease Models, Animal MeSH
• Rats, Wistar * MeSH
• Probiotics * administration & dosage   pharmacology   MeSH
• RNA, Ribosomal, 16S genetics   MeSH
• Triglycerides blood   metabolism   MeSH
• Bile Acids and Salts metabolism   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Humans MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Geographicals
• Iran MeSH
• Names of Substances
• Anti-Bacterial Agents MeSH
• Cholesterol 7-alpha-Hydroxylase MeSH
• Cholesterol MeSH
• RNA, Ribosomal, 16S MeSH
• Triglycerides MeSH
• Bile Acids and Salts MeSH

A high-fructose intake (HFI) in food, sweetened beverages, and soft drinks appears to be one of the risk factors that worsens human metabolic and cardiovascular health, although the more accurate mechanism remains unclear. Hypertriglyceridemic (HTG) rats represent a suitable animal model of metabolic syndrome where the consumption of an HFI could have an additional aggravating impact. We aimed to study the effect of fructose on the heart functions. Male HTG rats had HFI or a standard diet for five weeks. Heart function was tested ex vivo on the perfused heart using the Langendorff technique. Isolated hearts underwent 25 min ischemia (I) and 30 min reperfusion (R). Left ventricular developed pressure (LVDP), ventricular premature beats, and dysrhythmias were monitored during R. At the end of the R, ventricular fibrillation (VF) was evoked electrically. Systolic blood pressure, glucose level, serum total cholesterol (TC), triglycerides (TAG), and thiobarbituric acid reactive substances (TBARS) in the kidney were determined. The LVDP showed a reduced return to the input values, the duration of VF in R increased, and the threshold for VF induction decreased. Serum TC, TAG, and kidney TBARS were increased. The effect of HFI on heart ventricular impairment was associated with the reduced threshold for induction of VF and aggravated dyslipidemia. The results point to the adverse impact of dietary high-fructose intake in rats with hypertriglyceridemia.

• Keywords
• aortic endothelium-dependent relaxation, heart function, high-fructose intake, hypertriglyceridemic rats, lipid profile,
• MeSH
• Fructose * adverse effects   MeSH
• Hypertriglyceridemia * physiopathology   complications   MeSH
• Rats MeSH
• Disease Models, Animal MeSH
• Rats, Wistar MeSH
• Heart * drug effects   physiopathology   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Fructose * MeSH