AKT1 and metabolic disease: Investigations of the underlying mechanisms have shown that downregulation of the level of expression of Miro1 after a continuous challenge with an HFD, leads to imbalance activation of MKK-JNK-IRS1307 downstream and inhibition of AKT-Foxo1 phosphorylation cascades, promotion of IKO mouse pancreatic islet insulin resistance, inflammatory response and metabolic disorders, thereby the resultant T2D (Figure 6).