Fig. 1
VAT and EAT alterations under obesity and T2DM. In non-obese and non-T2DM subjects, WAT and BAT deposits in both VAT and EAT serve as storages and buffers for fatty acids (FA), attenuators of glycaemia and dyslipidaemia, and as controllers of vascular tension and inflammation. However, under abnormal or excessive fat accumulation, WAT and BAT depots become thicker and dysfunctional. WAT hypertrophies and it saturates, releasing FA and pro-inflammatory factors (cytokines, chemokines, RAAS) towards circulation and myocardium, leading to immune cells (IC) infiltration, myocardial steatosis and insulin resistance. BAT becomes reduced, atrophied and inactive (UCP-1 negative), losing its protective anti-glycemic/dyslipemic and anti-inflammatory effects