Abstract: Pre-diabetic insulin resistance is associated with sub-clinical inflammation and concomitant increase in systemic C-reactive protein (CRP) levels. Type 2 diabetes mellitus (T2DM) patients register even higher chronic levels of inflammation, with excess circulating CRP originating from both typical hepatic synthesis, and also visceral white adipose tissue. In addition, infiltration of pro-inflammatory macrophages into the expanding fat, as obesity becomes morbid, contributes further to dysregulation and symptomatic disease (Stanimirovic et al., 2022). Most importantly, in diabetic individuals, a sustained and chronic inflammation is perpetuated in the presence of non-healing wounds and ulcers, with associated further increase in CRP (Dangwal et al., 2015).