Background: Apolipoprotein A-V (Apo A-V) gene has recently been identified as a new apolipoprotein involved in triglyceride metabolism. A single nucleotide polymorphism (SNP3) located in the gene promoter (-1131) was associated with triglyceride variation in healthy subjects. In type 2 diabetes the triglyceride level increased compared to healthy subjects. Hypertriglyceridemia is a risk factor for coronary artery disease. We aimed to examine the interaction between SNP3 and lipid profile and coronary artery disease (CAD) in Tunisian type 2 diabetic patients. Results: The genotype frequencies of T/T, T/C and C/C were 0.74, 0.23 and 0.03 respectively in non diabetic subjects, 0.71, 0.25 and 0.04 respectively in type 2 diabetic patients. Triglyceride level was higher in heterozygous genotype (-1131 T/C) of apo A-V (p = 0.024). Heterozygous genotype is more frequent in high triglyceride group (40.9%) than in low triglyceride group (18.8%) ; p = 0.011. Despite the relation between CAD and hypertriglyceridemia the SNP 3 was not associated with CAD. Conclusion: In type 2 diabetic patients SNP3 is associated with triglyceride level, however there was no association between SNP3 and coronary artery disease.

Circulating fatty acids (FA) have an endogenous or exogenous origin and are metabolized under the effect of many enzymes. They play crucial roles in many mechanisms: cell signaling, modulation of gene expression, etc., which leads to the hypothesis that their perturbation could be the cause of disease development. FA in erythrocytes and plasma rather than dietary FA could be used as a biomarker for many diseases. Cardiovascular disease was associated with elevated trans FA and decreased DHA and EPA. Increased arachidonic acid and decreased Docosahexaenoic Acids (DHA) were associated with Alzheimer’s disease. Low Arachidonic acid and DHA are associated with neonatal morbidities and mortality. Decreased saturated fatty acids (SFA), increased monounsaturated FA (MUFA) and polyunsaturated FA (PUFA) (C18:2 n-6 and C20:3 n-6) are associated with cancer. Additionally, genetic polymorphisms in genes coding for enzymes implicated in FA metabolism are associated with disease development. FA desaturase (FADS1 and FADS2) polymorphisms are associated with Alzheimer’s disease, Acute Coronary Syndrome, Autism spectrum disorder and obesity. Polymorphisms in FA elongase (ELOVL2) are associated with Alzheimer’s disease, Autism spectrum disorder and obesity. FA-binding protein polymorphism is associated with dyslipidemia, type 2 diabetes, metabolic syndrome, obesity, hypertension, non-alcoholic fatty liver disease, peripheral atherosclerosis combined with type 2 diabetes and polycystic ovary syndrome. Acetyl-coenzyme A carboxylase polymorphisms are associated with diabetes, obesity and diabetic nephropathy. FA profile and genetic variants of proteins implicated in FA metabolism could be considered as disease biomarkers and may help with the prevention and management of diseases.

Background: Platelet aggregation and advanced glycation end products (AGEs) and oxidative stress are known as key factors for the development of cardiovascular diseases and diabetic complications. In this context, fruit and vegetable consumption, good sources of antioxidant compounds have been largely reported as an effective way of preventing human against these diseases. The current study focuses on the evaluation of antioxidant, antiplatelet and anti-glycation activities of pomegranate (Punica granatum L.) flowers (PF), leaves (PL), peel (PP) juice (PJ) and seeds oil (PSO). Methods: Antioxidant activities was measured against ABTS radical and lipid peroxidation. Antiglycation activity was determined using the formation of AGE fluorescence intensity in the BSA/ribose system. Antiplatelet activity was measured in platelet rich plasma (PRP) against adenosine diphosphate (ADP), Collagen and arachidonic acid (AA). Results: PF extract displayed the highest antioxidant activity against ABTS and lipid peroxidation with IC₅₀ values of 0.7 mg/mL and 0.63 mg/mL respectively. For anti-glycation activity, PP, PF and PL inhibited moderately the pentosidine-like AGEs formation compared to positive controls with AGE-IC₅₀ value of 0.4 mg/mL. PJ and PSO haven’t any anti-AGE effect. All the extracts selectively inhibited platelet aggregation caused by one, two or three inducers in dose dependent manner. PF was the most potent inhibitor caused by all three inducers, with inhibitory effects ranging from 35.6 to 66.6%. PP and PJ exhibited antiplatelet effect against both ADP and collagen and PL and PSO only against AA. Conclusions: These results suggest that some pomegranate extracts exert potential in vitro anti-glycative and antiplatelet activities.

Lipoprotein metabolism is regulated by several key proteins, notably proprotein convertase subtilisin/kexin type 9 (PCSK9) and the low‐density lipoprotein receptor (LDLR). Punica granatum peel extract has been reported to exhibit lipid‐lowering properties; however, the underlying mechanisms of its action on lipid metabolism remain insufficiently characterized. In this study, the hydroethanolic extract of P. granatum peel (PPE) was found to be rich in phenolic compounds and exhibited strong antioxidant activity. Characterization by liquid chromatography coupled with diode array and multiple‐stage mass spectrometry (LC‐DAD‐MS ⁿ ) identified punicalin, pedunculagin I, and galloyl‐HHDP‐hexose as the main constituents. Similar to statin treatment, PPE exposure significantly upregulated PCSK9 and LDLR protein expression in cultured cells compared to untreated controls, though the effect was less pronounced than that observed with statins. These findings suggest that phenolic‐rich PPE may serve as a promising natural source for the development of therapeutic agents aimed at preventing cardiovascular diseases.

Background: There is increasing evidence that thrombomodulin (THBD) polymorphisms, along with inflammatory markers [i.e., C-reactive protein (CRP), fibrinogen, albumin], may increase the risk of acute myocardial infarction (AMI). The aim of the study was to investigate the role of the THBD −33G>A polymorphism (rs1042579) as a marker of AMI risk and to correlate it with serum levels of inflammatory markers. Methods: Case–control study of 277 AMI patients and 329 healthy controls. A binary logistic regression analysis was performed to evaluate the association between the parameters studied and AMI risk. Results: The frequencies of genotypes AA, GA, and GG of the THBD −33G>A polymorphism were 31.4%, 45.5%, and 23.1% in patients and 21.6%, 44.1%, and 34.3% in controls. A significant association was found between the AA genotype of the THBD −33G>A polymorphism (AA: OR = 2.011, 95% CI 1.561-3.074, P < .001) or A allele (A: OR = 1.725, 95% CI 1.493-2.510, P < .001) and AMI risk. A backward stepwise logistic regression method combining AMI status as the dependent variable and conventional risk factors (age, smoking, arterial hypertension (HTA), diabetes, dyslipidemia, CRP, albumin, fibrinogen, serum angiotensin converting enzyme (ACE) activity, serum malondialdehyde, conjugated dienes, glutathione peroxidase, cardiac troponin-I (cTnI) and THBD AA genotype) as independent variables showed that the most predictive risk factors for AMI were smoking, HTA, albumin, fibrinogen, CRP, ACE activity, cTnI, and the THBD AA-genotype with odds ratios of 2.942, 2.203, 2.352, 1.323, 1.652, 1.014, 2.105, and 3.781 respectively. The AA genotype was associated with increased diastolic blood pressure, CRP, ACE activity, and albumin levels. Conclusions: The study shows that the THBD -33G>A polymorphism should be included in the stratification of AMI risk.