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Related Concept Videos

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...
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...
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...
Insulin: Dosing Regimen and Adverse Effects01:16

Insulin: Dosing Regimen and Adverse Effects

Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
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...

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Related Experiment Video

Updated: May 24, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
11:10

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Published on: November 16, 2011

Insulin, IGF-1 and longevity.

Diana van Heemst1

  • 1Department of Gerontology and Geriatrics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, the Netherlands.

Aging and Disease
|March 8, 2012
PubMed
Summary
This summary is machine-generated.

The insulin and insulin-like growth factor signaling pathway significantly impacts longevity in invertebrates. While complex in mammals, this pathway

Keywords:
IGF-1Insulinlongevitysignaling

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Last Updated: May 24, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
11:10

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Published on: November 16, 2011

A High-content In Vitro Pancreatic Islet &#946;-cell Replication Discovery Platform
09:35

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform

Published on: July 16, 2016

Area of Science:

  • Gerontology
  • Molecular Biology
  • Genetics

Background:

  • The insulin and insulin-like growth factor signaling (IIS) pathway is evolutionarily conserved.
  • IIS pathway mutations extend lifespan and promote youthful activity in invertebrates like C. elegans and D. melanogaster.
  • Mammalian IIS signaling is more complex, involving multiple receptors and ligands, complicating longevity research.

Purpose of the Study:

  • To explore the role of the insulin and insulin-like growth factor signaling (IIS) pathway in longevity.
  • To compare IIS pathway function in invertebrates and mammals regarding lifespan.
  • To investigate the potential relevance of IIS signaling in human longevity.

Main Methods:

  • Review of existing studies on IIS pathway mutations and lifespan in model organisms.
  • Comparative analysis of IIS pathway complexity across species.
  • Examination of genetic and metabolic factors associated with human longevity.

Main Results:

  • Reduced IIS signaling demonstrably increases lifespan in invertebrates.
  • Mouse models with decreased GH/IGF-1 or insulin signaling show enhanced lifespan.
  • The complexity of the mammalian IIS system hinders definitive conclusions on its role in longevity.

Conclusions:

  • The conserved IIS pathway is a key regulator of longevity in invertebrates.
  • While evidence suggests a role in mammalian lifespan, further research is needed due to system complexity.
  • Studies on human longevity hint at the conserved IIS pathway's potential involvement.