Then, to explore the mechanism-related results obtained in this cross-sectional cohort, we studied the effect of physiologically pertinent doses of uric acid, insulin, and their combination in two well-established in vitro models of diabetes-related LGI, i.e. lipopolysaccharide (LPS)-induced inflammation in monocytes and hyperglycaemia-stimulated endothelial cells [31, 32]. This evidence concerns the gene INS and Hyperglycemia.