Integration of FAM19A5 Expression, Plasma Atherogenic Index and Coronary Artery Histopathology in Diet-Induced Obese Rats

Background and Objective: Subclinical atherosclerosis in obesity is often not detected early. The FAM19A5 is a novel adipokin that is atheroprotective, known to play a role in inhibiting the proliferation and migration of Vascular Smooth Muscle Cells (VSMC), but its expression in adipose tissue and its association with vascular lesions remain unclear. The Plasma Atherogenic Index (PAI) is also a predictive indicator of cardiovascular risk, but its association with coronary histopathological changes has not been widely evaluated experimentally. The study assesses the relationship between FAM19A5 levels and expression, as well as PAI values, with the histopathological picture of coronary arteries in the obesity model Rattus induced by a high-fat and high-fructose diet. Materials and Methods: Fourteen male Sprague Dawley rats were divided into a control group (standard feed) and an obesity group (a high-fat and high-fructose diet for 12 weeks). An examination of FAM19A5 levels (ELISA), expression of mRNA FAM19A5 in adipose tissue (qRT-PCR), plasma lipid levels, PAI calculations and histopathological examination of coronary arteries. All analyses were conducted using SPSS version 25 and a p-valueResults: Circulating FAM19A5 levels were slightly higher in the obese group than in the control group, but not statistically significant. The expression of mRNA FAM19A5 is not detected in adipose tissue. The PAI value was higher in the obesity group. There was a significant difference in FAM19A5 levels in circulation between groups of coronary artery histopathological scores (pConclusion: The integration of FAM19A5 levels, PAI values and the histopathological picture of coronary arteries provides a preliminary understanding of the progression of subclinical atherosclerosis in obesity. The findings of undetected FAM19A5 mRNA expression support the hypothesis that FAM19A5 is not the primary adipokine and that its role in atherosclerosis is likely systemic or compensatory in nature.