Chokeberry Anthocyanin Extract as Pancreatic β-Cell Protectors in Two Models of Induced Oxidative Stress

Figure 2

Schematic illustration of CAE-stimulated antioxidant enzyme and insulin secretion pathway in pancreatic β-cells in HG and H₂O₂ stress conditions. Glucose enters the cell across the plasma membrane through glucose transporters, like GLUT-2 for rodent β-cells. Once inside the cell the metabolic process of glucose called glycolysis begins. ATP is the end product of glycolysis. Further reactions take place in mitochondria where more ATP is produced. In connection with the electron transport chain the superoxide anion results. Cytosolic or mitochondrial forms of SOD catalyze the conversion of superoxide anion () to molecular oxygen (O₂) and hydrogen peroxide (H₂O₂). Unlike glucose, H₂O₂ administered to cells diffuses through the cell membrane. The resulting H₂O₂ from glucose metabolism and the extracellular H₂O₂ are then metabolized to harmless water and oxygen by CAT and GPx. CAE increases the activity of SOD, CAT, and GPx, so the more active the metabolism of H₂O₂ is, the less the reactive species are formed in the cell. GSH levels are reduced by H₂O₂ and HG and restored by CAE. It is possible that the anthocyanins increase the insulin gene expression, because the CAE treatment attempts to restore the pool of insulin. Before being secreted out of the cell insulin is synthesized and converted to proinsulin in the endoplasmic reticulum (ER) folded and transported to the Golgi apparatus. Anthocyanins from CAE could also influence the opening of the voltage-gated Ca²⁺ channels, leading to an increased fusion of insulin granule with the cell membrane.