The glucose transporter isoform GLUT2 is expressed in liver, intestine, kidney and pancreatic islet beta cells, as well as in the central nervous system, in neurons, astrocytes and tanycytes.
First-pass extracted concept
GLUT2
Candidate: concept label1 source documents8 linked claims
Live refresh every 5sNext refresh in 5s
Aliases
Slc2a2
Evidence Snippets
Supporting Sources
Linked Claims
A missense mutation in GLUT2 is associated with preference for sugar-containing foods.
Quoted textsource-backed
Individuals with a missense mutation in GLUT2 show preference for sugar-containing foods.
Electrophysiological and optogenetic techniques established that Glut2-expressing neurons in the nucleus tractus solitarius are activated by hypoglycaemia and stimulate glucagon secretion.
Quoted textsource-backed
Electrophysiological and optogenetic techniques established that Glut2 (also known as Slc2a2)-expressing neurons of the nucleus tractus solitarius can be activated by hypoglycaemia to stimulate glucagon secretion.
GLUT2 is required for glucose-stimulated insulin secretion in pancreatic beta cells.
Quoted textsource-backed
In pancreatic beta cells, GLUT2 is required for glucose-stimulated insulin secretion.
GLUT2 variants are reported to increase risk of fasting hyperglycaemia, transition to type 2 diabetes, hypercholesterolaemia, and cardiovascular diseases.
Quoted textsource-backed
Genome-wide association studies have reported that GLUT2 variants increase the risks of fasting hyperglycaemia, transition to type 2 diabetes, hypercholesterolaemia and cardiovascular diseases.
Inactivating mutations in GLUT2 cause Fanconi-Bickel syndrome, and GLUT2 mutations can cause transient neonatal diabetes.
Quoted textsource-backed
In humans, inactivating mutations in GLUT2 cause Fanconi-Bickel syndrome, which is characterised by hepatomegaly and kidney disease; defects in insulin secretion are rare in adult patients, but GLUT2 mutations cause transient neonatal diabetes.
Liver GLUT2 expression is required for physiological control of glucose-sensitive genes and for maintaining normal glucose-stimulated insulin secretion through a liver-beta cell axis likely involving bile acids.
Quoted textsource-backed
GLUT2 expression is nevertheless required for the physiological control of glucose-sensitive genes, and its inactivation in the liver leads to impaired glucose-stimulated insulin secretion, revealing a liver-beta cell axis, which is likely to be dependent on bile acids controlling beta cell secretion capacity.
Suppression of GLUT2 expression in hepatocytes revealed an alternative glucose output pathway that may depend on membrane traffic.
Quoted textsource-backed
In hepatocytes, suppression of GLUT2 expression revealed the existence of an unsuspected glucose output pathway that may depend on a membrane traffic-dependent mechanism.
GLUT2-dependent glucose sensing in the nervous system controls feeding, thermoregulation, pancreatic islet cell mass and function, and autonomic activities.
Quoted textsource-backed
In the nervous system, GLUT2-dependent glucose sensing controls feeding, thermoregulation and pancreatic islet cell mass and function, as well as sympathetic and parasympathetic activities.