Potential effect of chronic Helicobacter pylori infection on glucose metabolism of Mongolian gerbils

Figure 6 Insulin-like growth factor-1 signaling with regard to Helicobacter pylori associated glucose dysregulation. Insulin-like growth factor-1 (IGF-1), upon binding to its receptor IGF-1R, activates the intrinsic tyrosine kinase activity. IGF-1R then phosphorylates substrate proteins, including members of the IRS family such as IRS1 and Shc on selective tyrosine residues. Downstream to the receptors are two major pathways: the phosphatidylinositol-3 kinase (PI3K)/Akt pathway and MAPK pathway. IGF-1 acts via the MAPK pathway to mediate growth responses. The PI3K pathway is thought to have predominantly metabolic effects. We supposed that this pathway might play a part in Helicobacter pylori (H. pylori) associated abnormal glucose metabolism and the upregulation of HbA1c. SHC: Spontaneous human combustion.