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Related Concept Videos

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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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: The Receptor and Signaling Pathways01:28

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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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Overview of Secretory Vesicles01:33

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Related Experiment Video

Updated: Jun 7, 2026

Confocal Imaging of Neuropeptide Y-pHluorin: A Technique to Visualize Insulin Granule Exocytosis in Intact Murine and Human Islets
09:41

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Published on: September 13, 2017

Toxins that modulate ionic channels as tools for exploring insulin secretion.

Carlos Manlio Diaz-Garcia1, Carmen Sanchez-Soto, Marcia Hiriart

  • 1Instituto de Fisiología Celular, Neuroscience Division, Department of Neurodevelopment and Physiology, Universidad Nacional Autónoma de México, Ciudad Universitaria, AP 70-253 Coyoacán, 04510 Mexico, DF, Mexico.

Cellular and Molecular Neurobiology
|November 4, 2010
PubMed
Summary
This summary is machine-generated.

Venom toxins offer insights into insulin secretion by targeting ion channels crucial for pancreatic beta-cell function. This research explores their potential for studying diabetes and developing new therapies.

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Last Updated: Jun 7, 2026

Confocal Imaging of Neuropeptide Y-pHluorin: A Technique to Visualize Insulin Granule Exocytosis in Intact Murine and Human Islets
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Published on: September 13, 2017

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Published on: June 25, 2019

Area of Science:

  • Endocrinology and Pharmacology
  • Toxinology and Molecular Physiology

Background:

  • Glucose-induced insulin secretion is vital for glucose homeostasis; its disruption can lead to type-2 diabetes mellitus.
  • Understanding insulin secretion mechanisms is crucial for developing new therapeutic agents.

Purpose of the Study:

  • To review the properties of toxins affecting ion channels involved in insulin secretion.
  • To highlight the utility of these toxins in studying pancreatic beta-cell physiology and developing novel therapeutics.

Main Methods:

  • Review of scientific literature on toxins affecting ion channels.
  • Examination of toxinology's contributions to understanding insulin secretion.
  • Analysis of ion channel composition in various cell models and primary cultures.

Main Results:

  • Toxins from venomous organisms significantly impact membrane excitability and ion channel function.
  • Toxinological studies have elucidated the ionic basis of insulin secretion and beta-cell ion channel composition.
  • A diverse array of toxins influencing insulin release has been identified.

Conclusions:

  • Venom-derived toxins are valuable tools for investigating pancreatic beta-cell function and insulin secretion.
  • These toxins hold significant potential for the development of novel pharmacological agents for diabetes treatment.