This scoping review aims to clarify the interplay between obesity, vitamin D deficiency, cellular senescence, and obesity-related metabolic consequences, mainly subclinical atherosclerosis, and non-alcoholic fatty liver disease (NAFLD). Obesity is a significant global health problem that involves cellular, environmental, behavioral, and genetic elements. The fundamental cause of obesity throughout all life stages is an energy imbalance, and its consequences are countless and, foremost, very common. Obesity has been comprehensively studied in the literature given its association with low serum vitamin D, with many proposed mechanisms linking the two conditions. Moreover, markers of exaggerated cellular senescence have been proven to accumulate in obese individuals. Subclinical atherosclerosis initiates an early stage that ends in serious cardiac events, and obesity, low vitamin D, and senescent cells largely contribute to its associated chronic low-grade inflammation. Furthermore, NAFLD signifies the hepatic manifestation of metabolic syndrome, and studies have highlighted the important role of obesity, vitamin D deficiency, and cellular senescence in its development. Therefore, we outlined the most important mechanisms tying these conditions to one another.

The aim of this study is to evaluate the changes in the inflammatory mediator’s serum amyloid A (SAA), adiponectin, and resistin in the serum of patients with stable angina and acute myocardial infarction. The study was done on 60 subjects divided into three groups: 20 healthy normal individuals as a control group, 20 patients with stable angina (atherosclerotic plaque), and 20 patients with myocardial infarction. Fasting blood samples were withdrawn from all subjects and serum was prepared. SAA, resistin, and adiponectin levels were quantitatively measured by enzyme-linked immunosorbent assay (ELISA). The SAA level was significantly higher in both stable angina and the acute myocardial infarction group than the control group (2.7179 ± 0.44501 mg/L) and the serum resistin level was significantly higher (p-value = 0.0) in the stable angina (8.368 ± 1.633 ng/ml) and the acute myocardial infarction (13.606 ± 2.067 ng/ml) groups (p-value= 0.0) than the control group. (2.4272±1.25210 ng/ml). Moreover, resistin levels in stable angina when compared to the AMI showed a significant difference between them (p-value = 0.0) while adiponectin was significantly lower in the acute myocardial infarction group. (6.641±2.6011 µg/mL, p-value = 0.019) than its level in the control group (11.873±1.798 µg/mL). While the adiponectin level showed no significant differences between stable angina in comparison to the AMI. SAA can be used as a confirmatory marker for stable angina and a diagnostic tool for AMI patients. Both SAA and resistin may participate in the atherosclerosis process as an effectors molecule of inflammatory reactions. For adiponectin, we concluded that it has the antiatherogenic property and its levels were lower in both the stable angina and acute myocardial infarction groups.

Background and Aim: Atherosclerosis is a chronic systematic disease where lesion (plaque) develops results in activation of inflammatory reaction that leads to arterial obstruction. Atherosclerosis is the underlying cause for many cardiovascular diseases (CVD) which were estimated with 42 percent of total death in Saudi Arabia while Coronary artery diseases (CAD) accounted for 35 percent of total chronic diseases death in Saudi Arabia by 2008. Risk factors that attribute in progression of atherosclerotic lesion and subsequent complications are smoking, high Low Density Lipoprotein –Cholesterol (LDL-C), high blood pressure, obesity and alcohol. Materials and Methods: This study was carried on 20 healthy individuals as a control group, 15 patients with stable angina, 15 patients with recent myocardial infraction (MI) and 15 patient 24-hours post MI. All subjects were males with age 45±65 years and underwent exclusion/inclusion criteria. COX-2, MMPs levels were quantitatively measured by enzyme-linked immunosorbent assay (ELISA). Results: There is insignificant differences in both COX-2 and MMP-2 levels among studied groups (P = 0.450 and 0.246 respectively) .On other hand, MMP-9 demonstrate a significant elevation in its level in studied groups (P = 0.014): its level significantly increase in stable angina (31.474 ± 12.188 ng/ml) compared to both control (9.920 ± 0.075 ng/ml) and Post MI groups (16.012 ± 13.852 ng/ml) (P = 0.001 and 0.004 respectively) and significantly increase in MI group (26.020 ± 14.792 ng/ml) when compared to both control (P = 0.006) and post MI (P = 0.038) groups. Conclusion: We can conclude that both COX-2 and MMP-2 cannot be used as markers for diagnosis of stable angina or MI. While MMP-9 as it showed significant elevation in its level in MI and then decrease in post MI, it can be considered as a good marker for confirming the diagnosis of MI and post MI stage.