Hypoxia in Obesity and Diabetes: Potential Therapeutic Effects of Hyperoxia and Nitrate

Figure 1

Insulin resistance in obesity. Obesity is associated with hypoxia, inflammation, and lipolysis. These conditions can lead to insulin resistance by impairment of insulin receptor substrate (IRS)/phosphatidyl inositol-3 kinase (PI3K)/AKT pathway. The c-Jun amino-terminal kinase (JNK), Toll-like receptors (TLRs), Akt substrate of 160 kDa (AS160), and AKT/serine (Ser)-1177 are the sensing points that hypoxia and inflammatory factors can inhibit insulin signaling. It should be noted that not all the above signaling occurs in every cell. GLUT: glucose transporter; IKKB: IκB kinase β; IR: insulin receptor; mTORC: mammalian target of rapamycin complex; PDK1: 3-phosphoinositide-dependent protein kinase 1; Ser307: serine 307; TNF-α-R: tumor necrosis factor-α receptor; Tyr P: phosphorylated tyrosine.