Fig. 1Regulation of the pancreatic β-cell mass dynamics.
Fig. 2Regulation of the pancreatic β-cell by peroxisome proliferator-activated receptor-gamma (PPARγ). RXR, retinoid X receptor; GLP-1R, glucagon-like peptide-1R; PI3K, phosphatidylinositol-3 kinase; IRS, insulin receptor substrate; PDX-1, pancreas duodenum homeobox-1; GLUT2, glucose transporter 2.
Fig. 3Regulation of the pancreatic β-cell by glucagon-like peptide-1 (GLP-1). GLUT2, glucose transporter 2; K-ATP, ATP-sensitive potassium channel; TCA, tricarboxylic acid; EGFR, epidermal growth factor receptor; VDCC, voltage-dependent calcium channels; PI3K, phosphatidylinositol-3 kinase; IRS, insulin receptor substrate; PKC, protein kinase C; MAPK, mitogen-activated protein kinase; ER, endoplasmic reticulum; cAMP, cyclic adenosine monophosphate; PKA, protein kinase A; AC, adenylate cyclase; Epac, exchange protein activated by cAMP.
Fig. 4Insulin-induced inactivation of glycogen synthase kinase 3 β (GSK3β). IRS, insulin receptor substrate; PI3K, phosphatidylinositol-3 kinase.
Fig. 5Regulation of the pancreatic β-cell by G protein-coupled receptor 40 (GPR40). GLUT2, glucose transporter 2; K-ATP, ATP-sensitive potassium channel; TCA, tricarboxylic acid; VDCC, voltage-dependent calcium channels; PLC, phospholipase C; DAG, diacylglycerol; PKC, protein kinase C; IP3, 1,4,5-trisphosphate; PIP2, 4,5-bisphosphate; ER, endoplasmic reticulum; cAMP, cyclic adenosine monophosphate; PKA, protein kinase A; Epac, exchange protein activated by cAMP; AC, adenylate cyclase; GLP-1, glucagon-like peptide-1.
Table 1Therapeutic approaches for maintaining β-cell function and mass in animal and human data