Structure, function, and regulation of the mammalian facilitative glucose transporter gene family

Ann Louise Olson, Jeffrey E. Pessin

Research output: Contribution to journalArticle

326 Citations (Scopus)

Abstract

The facilitative transport of glucose across the plasma membranes of mammalian cells is catalyzed by a family of glucose transport proteins (GLUT). Four glucose transport proteins and a fructose transport protein have been identified. These transport proteins have unique tissue distributions and biochemical properties under- lying specific physiologic functions. GLUT1, the first GLUT isoform identified, is expressed at highest levels in the endothelial of harrier tissues such as blood vessels and the blood-brain barrier. GLUT2, found predominantly in liver, intestine, kidney, and pancreatic β-cells, is a low-affinity glucose transport protein that is part of the glucose sensor in pancreatic β-cells and facilitates either glucose uptake or efflux from the liver depending on the nutritional state. GLUT3 is the glucose transporter responsible for maintaining an adequate glucose supply to neurons. GLUT4 is the insulin-regulated glucose transporter found in adipose tissues, heart muscles, and skeletal muscles that is responsible for insulin-regulated glucose disposal.

Original languageEnglish (US)
Pages (from-to)235-256
Number of pages22
JournalAnnual Review of Nutrition
Volume16
StatePublished - 1996
Externally publishedYes

Fingerprint

Facilitative Glucose Transport Proteins
Glucose
Genes
Carrier Proteins
Insulin
Liver
Tissue Distribution
Fructose
Blood-Brain Barrier
Endothelium
Intestines
Blood Vessels
Adipose Tissue
Myocardium
Protein Isoforms
Skeletal Muscle
Cell Membrane
Kidney
Neurons

Keywords

  • GLUT1
  • GLUT2
  • GLUT3
  • GLUT4
  • insulin

ASJC Scopus subject areas

  • Medicine (miscellaneous)

Cite this

Structure, function, and regulation of the mammalian facilitative glucose transporter gene family. / Olson, Ann Louise; Pessin, Jeffrey E.

In: Annual Review of Nutrition, Vol. 16, 1996, p. 235-256.

Research output: Contribution to journalArticle

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