File:Ijms-21-06286-g004-550.webp

English: Figure 4. GLUT2-mediated glucose transport across cell membranes and communication to different organs. GLUT2 is a low affinity and high capacity glucose transporter and facilitates the transport of glucose in intestinal cells. SGLTs are high-affinity and low capacity transporters, capable of transporting glucose against a concentration gradient. Ghrelin increases the GLUT2 expression by modulating the GLUT2 transcription via GHS-R1 (growth hormone secretagogue receptor 1a) and PLC/PKC pathway. Ghrelin also stimulates translocation of GLUT2 to the surfaces of intestinal cell from intracellular vesicles, leading to increased glucose absorption. GLUT2 is highly expressed in the liver, pancreas, brain and kidney cells. Activation of nervous signals, induces the first phase of insulin release from pancreatic β-cells induced by increased glucose transport to pancreatic β-cells. These signals also induce other physiological processes. In the liver, GLUT2 maintains the glucose homeostasis during fasting and fed state by regulating the expression of glucose-sensitive genes. GLUT2 is more highly expressed in rodent β-cells than in human β-cells. In the brain, glucose-sensing cells expressing GLUT2, regulate glucose by parasympathetic and sympathetic systems. GLUT2-dependent glucose-sensing cells also regulate leptin sensitivity and regulate the expressions of uncoupling protein 1 (UCP1) and thermogenesis. Homozygous GLUT2 mutation leads to a dysfunctional and reduced expression of GLUT2, which causes FBS. Dysfunctional GLUT2 causes fasting hypoglycemia, postprandial hyperglycemia, glucose and galactose intolerance, hepatomegaly, glucosuria, reduced GSIS (glucose-stimulated insulin secretion), rickets, GH (growth hormone) deficiency and poor, growth. (G; glucose).