PCSK-9 modulation by oral administration of Berberine using nanotechnology approach can improve its pharmacokinetic profile. Further studies are needed to maximize its delivery efficiency.

Depression is an independent risk factor of cardiovascular disease morbidity. Serotonin is a key neurotransmitter in depressive pathology, contained within platelets, and is a weak activator of platelets. Our study assessed the link between platelet reactivity traits, depression, and antidepressant (AD) use in a large population sample. Our study was conducted in the Framingham Heart Study (n = 3,140), and AD use (n = 563) and aspirin use (n = 681) were noted. Depression was measured using the Center for Epidemiological Studies-Depression (CES-D) survey. Platelet reactivity traits were measured across multiple agonists using five distinct assays. We utilized a linear mixed effects model to test associations between platelet traits and depression, adjusting for age, sex, aspirin use, and AD use. Similarly, we analyzed trait associations with any AD use, serotonin-affecting ADs, and norepinephrine-affecting ADs, respectively. There were strong associations with reduced platelet function and AD use, particularly with serotonin-affecting medications. This included lower Optimul epinephrine maximal aggregation (P = 4.87E-13), higher U46619 half maximal effective concentration (P = 9.09E-11), lower light transmission aggregometry (LTA) adenosine diphosphate (ADP) final aggregation (P = 1.03E-05), and higher LTA ADP disaggregation (P = 2.28E-05). We found similar associations with serotonin-affecting ADs in an aspirin-taking subset of our sample. There were no significant associations between platelet traits and depression. In the largest study yet of AD use and platelet function we show that antidepressants, particularly serotonin-affecting ADs, inhibit platelets. We did not find evidence that depressive symptomatology in the absence of medication is associated with altered platelet function. Our results are consistent with AD use leading to platelet serotonin depletions, decreased stability of platelet aggregates, and overall decreased aggregation to multiple agonists, which may be a mechanism by which ADs increase risk of bleeding and decrease risk of thrombosis.

Introduction Triglyceride (TG) is an independent risk factor for coronary heart disease. Previous work has shown that short-term supplementations of mouse chow with oxidized linoleic acid (OxLA) significantly reduce the level of plasma triglycerides. Study Objective This study aims to determine the effects of longer-term supplementation of mouse chow with various concentrations of oxidized linoleic acid (OxLA) on plasma triglycerides. Study Design The study consisted of forty C57BL/6 wildtype mice divided into four groups (n = 10). Two groups were kept as controls. One control group (P) was fed plain chow and the second control group (C) was fed chow supplemented with linoleic acid. The other two experimental groups (A) and (B) were fed oxidized linoleic acid supplemented chow in the following doses: 9 mg/day of oxidized linoleic acid and 18 mg/day of oxidized linoleic acid/mouse. Results and Conclusion Mice that were on a diet supplemented with the higher dose of oxidized linoleic acid showed a 39% decrease in hepatic PPAR-α and a significant decrease in the plasma HDL levels compared to the mice that were fed diets of plain and linoleic acid supplemented chow. Interestingly, the longer-term consumption of oxidized linoleic acid may predispose to atheropathogenesis.

Introduction: FGF-23 is a phosphatouric hormone which also serves as a plasma biomarker that mediates pathologic cardiac remodeling, such as left ventricular hypertrophy or myocardial fibrosis, and is associated with increased cardiovascular mortality. However, limited evidence is available on lifestyle-related factors associated with circulating concentration of this emerging cardiovascular risk factor. Objective: Our aim was to measure the association between the American Heart Association’s Life’s Simple 7 (LS7) and circulating FGF-23 concentration among Puerto Rican adults. Methods: Data are from Boston Puerto Rican Health Study (BPRHS) participants (mean age 56.2 years, 77% female) at baseline and at approximately 8-y follow-up (n=410). LS7 was calculated at baseline and includes 4 physiological (BMI, total cholesterol, blood pressure, and fasting glucose) and 3 behavioral factors (smoking, physical activity, and diet). Each component was categorized using a constituent scoring system (ideal=2; intermediate=1; Poor=0) and these were summed to calculate the total LS7 score. Participants were categorized into 5 LS7 groups as follows: 1) score 1-4 (n=105), 2) 5 (n=76), 3) 6 (n=89), 4) 7 (n=69), and 5) 8-12 (n=71). Fasting plasma FGF-23 concentration at 8-y follow-up was measured by ELISA. Associations between baseline LS7 score and 8-y FGF-23 were assessed using ANCOVA, adjusted for age and sex (model 1), and additionally for history of cardiovascular disease and poverty-income-ratio (model 2). Results: Relative to participants in LS7 group 1 (2.98 ± 1.09 mg/dL), those in groups 5 (1.63 ± 1.12 mg/dL, p=0.0001) had significantly lower FGF-23 concentration (model 1, P-trend=0.0001). After considering additional confounders, FGF-23 concentration among LS7 group 5 (1.69 ± 1.12 mg/dL, p=0.0007) remained significantly lower than in group 1 (2.95 ± 1.09 mg/dL). The p-trend across categories was also significant at p=0.0007. In additional analyses, LS7 components for smoking (ideal vs. poor, 2.07 ± 1.10 mg/dL vs. 2.87 ± 1.10 mg/dL, p=0.01) and fasting glucose (ideal vs. poor, 2.03 ± 1.07 mg/dL vs. 2.90 ± 1.09 mg/dL, p=0.004), but no other components, were associated with FGF-23 concentration. Conclusions: Optimal LS7 status was associated with lower 8-y mean plasma FGF-23 concentration. Efforts to target LS7 components, particularly smoking and glucose control, may improve FGF-23 concentration among Puerto Rican adults.

No abstract