Abstract Body: Introduction
Cardiovascular diseases (CVDs) continue to pose a significant global health challenge, with vitamin D deficiency and obesity emerging as prominent risk factors. Arterial stiffness is recognized as a pivotal predictor and an independent risk element for CVDs. This study explores the metabolomic profiling of blood samples obtained from individuals afflicted with early arterial stiffness due to vitamin D deficiency and obesity, compared with a control group.
Methods
The study comprised nine participants with vitamin D deficiency (vitamin D level of 20 ng/ml or lower), and obese participants (BMI of 30 or higher), along with eleven control participants (with vitamin D levels above 20 ng/ml and normal BMI). Pulse Wave Velocity (PWV) measurements were conducted using the SphygmoCor device. Whole blood was collected from each participant in EDTA tubes, followed by centrifugation at 4200 RPM for 10 minutes to obtain plasma samples, which were then stored in a -80°C freezer. Metabolomic analysis was carried out using Liquid Chromatography coupled with tandem mass spectrometry (LC-MS/MS). A two-tailed p-value < 0.05 was considered statistically significant for all analyses.
Results
The average PWV value relative to the participant's age was 19.4 ± 4.7 m/s in the group with both vitamin D deficiency and obesity, compared to 14.7 ± 2.1 m/s in the control group (p < 0.05), indicating increased arterial stiffness. Furthermore, eleven metabolites exhibited statistically significant differences in patients with vitamin D deficiency and obesity. Of these, eight metabolites demonstrated increased expression levels, including Nutriacholic acid, N-Acetylputrescine, Succinylacetone, Adenosine monophosphate, Elaidic acid, Niacinamide, DUMP, and 2-Pyrrolidinone, while three metabolites exhibited decreased expression: PC (18:1(9Z)/18:1(9Z)), Trimethylamine, and Imidazole. Additionally, top enrichment analysis revealed metabolic pathways predicted to be altered in the context of dysfunctional enzymes, encompassing processes such as nicotinamide acid uptake, fatty-acyl-CoA synthase (n-C18:0CoA), and extracellular NADP nucleosidase, among others.
Conclusion
The metabolomic alterations identified in our study offer insights into potential biomarkers for evaluating arterial stiffness and present novel targets for therapeutic interventions in vitamin D deficient and obese individuals.