CRP and Insulin resistance: The pathophysiology of MHO is considered as subclinical adipose tissue inflammation that often results in insulin resistance and is measured by predictors including C-reactive protein, interleukin 6, and free fatty acid levels; transition of adipose tissue leading to a metabolic state; and regulatory genetic predisposition involving the processes of apoptosis, adipogenesis, angiogenesis, and dysregulation of epigenetic adaptation hypothesis [47].