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Related Concept Videos

Glucose Transporters01:27

Glucose Transporters

Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
Glucose Absorption Into the Small Intestine01:26

Glucose Absorption Into the Small Intestine

Complex carbohydrates consumed cannot be absorbed into the small intestine in their original form. First, they must be hydrolyzed to a monosaccharide form such as glucose or galactose. These monosaccharides are then transported across the intestinal membrane and into the blood via transcellular transport. The intestinal epithelial cells allow the movement of these monosaccharides with a defined 'entry' through membrane transporter proteins present on their apical membrane and 'exit' via the...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.

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Related Experiment Video

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Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
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GLUT2 mutations, translocation, and receptor function in diet sugar managing.

Armelle Leturque1, Edith Brot-Laroche, Maude Le Gall

  • 1Centre de recherche des Cordeliers 15 rue de l'école de médecine, F-75006 Paris, France. armelle.leturque@crc.jussieu.fr

American Journal of Physiology. Endocrinology and Metabolism
|February 19, 2009
PubMed
Summary

GLUT2, a glucose transporter, plays a key role in sugar sensing and transport. Recent findings reveal its impact on metabolic diseases and cellular functions, independent of glucose metabolism.

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Area of Science:

  • Molecular biology
  • Metabolic diseases
  • Cellular physiology

Background:

  • GLUT2 is a low-affinity, high-capacity glucose transporter found in various organs, including the liver, pancreas, intestine, kidney, and brain.
  • Historically, GLUT2's role in human metabolic diseases was considered minor.
  • Gene expression of GLUT2 is influenced by sugars and hormones.

Purpose of the Study:

  • To review recent discoveries concerning the GLUT2 protein in health and metabolic disease.
  • To highlight the newly revealed functions of GLUT2, including its role in genetic disorders, sugar preferences, and cellular signaling.
  • To identify unanswered questions regarding GLUT2's multifaceted roles.

Main Methods:

  • Review of recent scientific literature and research findings on GLUT2.
  • Analysis of genetic studies identifying GLUT2 mutations and polymorphisms.
  • Examination of studies investigating GLUT2's cellular localization and signaling functions.

Main Results:

  • GLUT2 mutations cause Fanconi-Bickel syndrome, a rare glycogenosis. A GLUT2 polymorphism is linked to sugary food preferences.
  • GLUT2's cell surface localization is regulated, impacting sugar uptake in enterocytes and potentially other organs.
  • GLUT2 acts as a sugar sensor, detecting extracellular sugars to modulate insulin secretion, renal, and intestinal absorption.

Conclusions:

  • Recent research has significantly expanded our understanding of GLUT2's functions beyond simple glucose transport.
  • GLUT2 plays critical roles in metabolic regulation, cellular signaling, and is implicated in specific genetic diseases and dietary preferences.
  • Further research is needed to fully elucidate the complex mechanisms and implications of GLUT2 in health and disease.