Cellular senescence and vitamin d deficiency play a role in the pathogenesis of obesity‐associated subclinical atherosclerosis: Study of the potential protective role of vitamin d supplementation

Abstract

The exact link between obesity, vitamin D deficiency, and their relation to cellular senescence in the pathogenesis of subclinical atherosclerosis is still under debate. Therefore, the current study aims to verify the possible role of vitamin D deficiency and cellular senescence in the pathogenesis of obesity‐related subclinical atherosclerosis. Moreover, it aims to investigate the possible protective role of vitamin D supplementation. Fifty‐seven male albino rats were enrolled in the study and classified into four groups: negative (10) and positive control groups (10), an obese model group (24), and a vitamin‐D‐supplemented obese group (13). Aortic tissue samples and fasting blood samples were collected. The following biochemical investigations were performed: serum cholesterol, triglycerides, HDL‐C, LDL‐C, ALT, AST, CPK, CK‐MB, and hs‐cTnt. HOMA‐IR was calculated. Moreover, serum SMP‐30, 25 (OH)Vitamin D3, and eNOS were determined by the ELISA technique. Aortic gene expression of eNOS, SMP‐30, and P53 was estimated by real‐time qRT‐PCR. Serum 25(OH) D3 and SMP‐30 were lower in the obese group. In addition, the obese group showed higher serum lipid profile, HOMA‐IR, eNOS, ALT, AST, CPK, CK‐MB, and hs‐cTnt than the control groups, while decreased levels were found in the vitamin‐D‐treated obese group. Gene expression of eNOS and SMP‐30 were in accordance with their serum levels. A positive correlation was found between vitamin D level and SMP‐30. In conclusion, obesity is associated with vitamin D deficiency and enhanced cellular senescence. They could play a role in the pathogenesis of obesity‐associated subclinical atherosclerosis and endothelial dysfunction. Vitamin D supplements could play a protective role against such obesity‐related comorbidity.