“…Hence, these physiopathological mechanisms are expressed in obesity-associated and metabolic defects in other tissues, such as atherogenic dyslipidemia, endothelial dysfunction and hypertension [59]. In this complex process, apart from obesity-associated insulin resistance, other metabolic factors play a key role in the evolution of MetS, including inflammatory factors [60], defects in the target cell (i.e., receiver and post-receiver) [2], and an increase in insulin counterregulatory hormones and anti-insulin antibodies (AIA) [61]. Consequently, endothelial dysfunction and dyslipidemia leads to atherosclerotic mechanisms and arterial intima-media thickness [62,63], and, consequently, to an increased risk of micro and macrovascular complications in chronic disease, with a particular emphasis on T2DM [2], which explains the inclusion of SBP, DBP, TG and HDL in the harmonised definition of MetS [28].…”