In response to an excess energy supply, AT expansion leads to adipocyte hypertrophy (increase in size of existing adipocytes) and, in some cases, adipocyte hyperplasia (increase in the number of adipocytes recruited from adipose stromal cells) associated with fibrosis (with the accumulation of collagens 1 and 6) and hypoxia (with the induction of hypoxia-inducible-factor-1-alpha (HIF-1α)), leading then to AT dysfunction and progression towards insulin resistance [12,14]. Here, HIF1A is linked to Insulin resistance.