The clustering of cardiovascular risk factors in DM indicates that the multiple complex metabolic reactions involved in glycotoxicity
, lipotoxicity, altered insulin signaling, increased cytokine activity, and interstitial deposition of triacylglycerol may directly or indirectly affect CA function [15-17, 20].
Overall, the lipoperoxidation and MDA formation might be consequence of dysfunctional glycated proteins, AGEs, and glycooxidative stress glycol-oxidative stress (hyperglycemic glycotoxicity
) and consequence of lipotoxicity when lipid is forced into organ cells (e.g., liver, skeletal, and heart muscle and pancreas) significantly impairing functions.
In fact, NLRP3 inflammasomes have been proposed to sense and mediate downstream inflammatory events of glycotoxicity
and lipotoxicity during the pathogenesis of T2DM [45, 57].