Intracellular calcium channels: Potential targets for type 2 diabetes mellitus?

Figure 1 AMP-activated protein kinase activation in type 2 diabetes mellitus. In patients with type 2 diabetes mellitus, AMP-activated protein kinase promotes glucose transporter isoform 4 translocation from vesicles to the plasma membrane by inhibiting TBC1 domain family member 1, and inhibits liver gluconeogenesis by blocking the conversion of oxaloacetic acid to phosphoenolpyruvate and glucose-6-phosphate to free glucose, leading to reduced blood glucose. APMK: AMP-activated protein kinase; T2DM: Type 2 diabetes mellitus; GLUT4: Glucose transporter isoform 4.

Figure 2 Potential roles of calcium-permeable ion channels in glucose uptake. A working model to illustrate the possible role of calcium ion channels in glucose uptake. Various calcium ion channels located on various organelles and the plasma membrane can increase the cytosolic calcium release, then activating calmodulin-dependent protein kinase 2/AMP-activated protein kinase pathway via phosphorylation of the Thr172 site and leads to increased glucose uptake, thus treating type 2 diabetes mellitus (T2DM). Specific agonists could be potential therapeutic drugs for T2DM. PM: Plasma membrane; ER: Endoplasmic reticulum.