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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...
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...
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
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...
Synthesis and Functions of Calcitonin00:51

Synthesis and Functions of Calcitonin

Calcitonin, a vital polypeptide hormone, regulates calcium levels within body fluids. It is released by the parafollicular cells, also known as C cells, situated in the follicular epithelium of the thyroid gland. Calcitonin responds to fluctuations in blood calcium levels and the influence of gastrointestinal hormones like gastrin and cholecystokinin.
The exact mechanisms by which calcitonin operates in calcium homeostasis remain elusive, but its significance is evident in several vital...

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Related Experiment Video

Updated: Jun 15, 2026

Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells
08:03

Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells

Published on: November 26, 2019

Calcium signaling in the islets.

M Shahidul Islam1

  • 1Department of Clinical Sciences and Education, Södersjukhuset, Karolinska Institutet, Research Center, 118 83 Stockholm, Sweden. shaisl@ki.se

Advances in Experimental Medicine and Biology
|March 11, 2010
PubMed
Summary
This summary is machine-generated.

Rodent data on calcium (Ca2+) signaling in islets does not fully apply to humans. New research highlights distinct human beta-cell electrical activity and calcium signaling complexities crucial for diabetes understanding.

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Related Experiment Videos

Last Updated: Jun 15, 2026

Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells
08:03

Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells

Published on: November 26, 2019

Confocal Laser Scanning Microscopy of Calcium Dynamics in Acute Mouse Pancreatic Tissue Slices
10:49

Confocal Laser Scanning Microscopy of Calcium Dynamics in Acute Mouse Pancreatic Tissue Slices

Published on: April 13, 2021

Analysis of Beta-cell Function Using Single-cell Resolution Calcium Imaging in Zebrafish Islets
08:50

Analysis of Beta-cell Function Using Single-cell Resolution Calcium Imaging in Zebrafish Islets

Published on: July 3, 2018

Area of Science:

  • Endocrinology
  • Cell Physiology
  • Molecular Biology

Background:

  • Rodent islet and insulinoma cell data heavily influence human calcium (Ca2+) signaling understanding.
  • Extrapolation of rodent data, often from suboptimal conditions, may misrepresent human islet physiology.
  • Recent studies focus on human islets to clarify Ca2+ signaling mechanisms.

Purpose of the Study:

  • To elucidate the ion channel repertoire and relative importance in human islet Ca2+ signaling.
  • To investigate the complexity of Ca2+ signaling in human beta-cells, including novel channels and mechanisms.
  • To differentiate human islet physiology from rodent models for improved diabetes research.

Main Methods:

  • Electrophysiological studies of human islets.
  • Calcium imaging using fluorescent indicators in human beta-cells.
  • Analysis of ion channel expression and function in human pancreatic beta-cells.

Main Results:

  • Human beta-cells exhibit unique electrical activity and Ca2+ signaling patterns, differing from rodents.
  • Novel channels, including the transient receptor potential (TRP) family, are identified in human beta-cells.
  • Mechanisms like Ca2+-induced Ca2+ release (CICR) add complexity to human beta-cell Ca2+ dynamics.

Conclusions:

  • Human beta-cell physiology, including resting membrane potential (~ -50 mV) and insulin secretion patterns, is distinct from rodent models.
  • Biphasic insulin secretion is an artifact, not reflective of physiological pulsatile secretion.
  • Further research into human islet Ca2+ signaling is essential for understanding diabetes pathogenesis and developing treatments.