Chronic inflammation in obesity is primarily driven by the expansion of visceral adipose tissue, leading to adipocyte hypertrophy, hypoxia, and the recruitment of pro inflammatory immune cells such as M1 macrophages, contributing to elevated cytokines like tumor necrosis factor-alpha (TNF α), interleukin-6 (IL 6), and C reactive protein (CRP), which are central to insulin resistance, endothelial dysfunction, and hepatic steatosis [3,4,9]. This evidence concerns the gene CRP and obesity disorder.