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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...
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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.
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Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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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.
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Glucagon-like Receptor Agonists01:24

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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.
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Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively manages...

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Related Experiment Video

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Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
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Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion

Published on: May 10, 2018

Insulin action under arrestin.

Jacqueline Stöckli1, David E James

  • 1Garvan Institute of Medical Research, 384 Victoria St., Darlinghurst, NSW, Australia.

Cell Metabolism
|March 4, 2009
PubMed
Summary
This summary is machine-generated.

Beta-arrestin, a protein known for controlling receptor desensitization, plays a crucial role in insulin signaling. Beta-arrestin-2 specifically regulates insulin action by influencing the assembly of key signaling proteins in mouse models.

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Last Updated: Jun 25, 2026

Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
07:30

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Published on: May 10, 2018

Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat
11:12

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Published on: February 7, 2011

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
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Published on: November 16, 2011

Area of Science:

  • Biochemistry
  • Cellular signaling
  • Metabolic research

Background:

  • Insulin resistance is a central feature of metabolic syndrome.
  • Beta-arrestins are primarily known for their role in G protein-coupled receptor (GPCR) desensitization.
  • The involvement of beta-arrestins in non-GPCR pathways, such as insulin signaling, is an emerging area of research.

Purpose of the Study:

  • To investigate the role of beta-arrestin in insulin signaling.
  • To elucidate the specific function of beta-arrestin isoforms in the regulation of insulin action.

Main Methods:

  • Utilized mouse models to study whole-body insulin action.
  • Investigated the molecular mechanisms underlying beta-arrestin's role in insulin signaling.
  • Examined the assembly of protein complexes involved in insulin receptor signaling.

Main Results:

  • Beta-arrestin, particularly beta-arrestin-2, was found to be involved in insulin signaling.
  • Beta-arrestin-2 regulates whole-body insulin action in vivo.
  • Beta-arrestin-2 controls the assembly of a signaling complex including the insulin receptor, c-Src, and Akt.

Conclusions:

  • Beta-arrestin is a novel regulator of insulin signaling.
  • Beta-arrestin-2 is a key mediator of insulin action through the regulation of specific protein complex formation.