Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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...
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Reclassification of basic experimental studies in humans - a case for a new publishing consensus.

Nature metabolism·2026
Same author

Integrated analysis of insulin resistance reveals metabolic remodeling following diet switch-triggered calorie reduction.

Science advances·2026
Same author

The gut microbiome as an effector of metabolic disease gene variants.

Trends in genetics : TIG·2026
Same author

A PTPN23-dependent ESCRT pathway is essential for constitutive secretion in mammalian cells.

The Journal of cell biology·2026
Same author

Dynamic subcellular proteomics identifies regulators of adipocyte insulin action.

Nature communications·2026
Same author

Integrated analysis of the adipocyte plasma membrane proteome reveals KCC1 and PIT2 as novel insulin-responsive transporters.

The Journal of biological chemistry·2026
Same journal

Traffic Light Commentary-Src in the Upside Down: A Kinase Turned Inside Out.

Traffic (Copenhagen, Denmark)·2026
Same journal

Integrating Lateral Super-Resolution and Axial Progression Reveals Distinct Clathrin Pit Formation Pathways.

Traffic (Copenhagen, Denmark)·2026
Same journal

A Quarter Century of EHD Protein Research: From Endosomal Recycling to Ciliopathies.

Traffic (Copenhagen, Denmark)·2026
Same journal

Mechanistic Insight Into Clathrin-Mediated Endocytosis in Plants.

Traffic (Copenhagen, Denmark)·2026
Same journal

Clathrin-Mediated Endocytosis in Plants: Historical to Modern Advances.

Traffic (Copenhagen, Denmark)·2026
Same journal

A Toolbox for Quantifying Nuclear and Nucleolar Protein Accumulation Using NLS and NoLS Fusion Reporters.

Traffic (Copenhagen, Denmark)·2026
See all related articles

Related Experiment Video

Updated: Jun 3, 2026

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
08:47

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

Mapping insulin/GLUT4 circuitry.

Alexander F Rowland1, Daniel J Fazakerley, David E James

  • 1Diabetes and Obesity Program, Garvan Institute of Medical Research, Sydney, New South Wales 2010, Australia.

Traffic (Copenhagen, Denmark)
|March 16, 2011
PubMed
Summary
This summary is machine-generated.

Insulin stimulates glucose uptake by moving GLUT4 (glucose transporter type 4) to the cell surface. Understanding the key regulated steps in this complex trafficking process is crucial for metabolic research.

More Related Videos

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
08:03

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes

Published on: June 25, 2017

Detection of Detergent-sensitive Interactions Between Membrane Proteins
10:09

Detection of Detergent-sensitive Interactions Between Membrane Proteins

Published on: March 7, 2018

Related Experiment Videos

Last Updated: Jun 3, 2026

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
08:47

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
08:03

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes

Published on: June 25, 2017

Detection of Detergent-sensitive Interactions Between Membrane Proteins
10:09

Detection of Detergent-sensitive Interactions Between Membrane Proteins

Published on: March 7, 2018

Area of Science:

  • Cell biology
  • Molecular endocrinology
  • Metabolic signaling

Background:

  • Insulin is a key metabolic hormone regulating glucose uptake in muscle and fat cells.
  • Glucose transporter type 4 (GLUT4) translocation to the plasma membrane is a primary mechanism for insulin-stimulated glucose uptake.
  • The phosphatidylinositol-3-kinase/Akt pathway mediates insulin's action on GLUT4 trafficking.

Purpose of the Study:

  • To investigate the critical, regulated steps in insulin-stimulated GLUT4 translocation.
  • To identify molecular regulators of GLUT4 trafficking beyond TBC1D4.
  • To advocate for a systems-level approach to understand insulin signaling and GLUT4 traffic.

Main Methods:

  • Review of existing literature on insulin signaling and GLUT4 trafficking.
  • Analysis of the multi-step process of GLUT4 vesicle movement.
  • Discussion of the need for global modeling of signaling networks.

Main Results:

  • Insulin-stimulated GLUT4 translocation involves at least four distinct trafficking steps.
  • TBC1D4 is a known regulator, but molecular details for other distal signaling components remain unclear.
  • A comprehensive understanding requires dissecting how various molecules influence specific trafficking steps.

Conclusions:

  • Identifying the major regulated step in GLUT4 translocation is essential.
  • A global approach and detailed network modeling are needed to fully elucidate the molecular mechanisms controlling GLUT4 traffic.
  • This will reveal critical control nodes and emergent properties of the insulin signaling system.