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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...
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...
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
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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Related Experiment Video

Updated: Jun 3, 2026

Sustained Administration of &#946;-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres
09:31

Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres

Published on: November 5, 2016

Immobilization of soluble complement receptor 1 on islets.

Nguyen M Luan1, Yuji Teramura, Hiroo Iwata

  • 1Department of Reparative Materials, Institute for Frontier Medical Sciences, Kyoto University, Sakyo-Ku, Kyoto, Japan.

Biomaterials
|April 5, 2011
PubMed
Summary

Immobilizing human soluble complement receptor 1 (sCR1) on pancreatic islets protects them from immune attack. This breakthrough enhances islet transplantation success, paving the way for future xenotransplantation therapies.

More Related Videos

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

Related Experiment Videos

Last Updated: Jun 3, 2026

Sustained Administration of &#946;-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres
09:31

Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres

Published on: November 5, 2016

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

Area of Science:

  • Immunology
  • Transplantation Biology
  • Biomaterials Science

Background:

  • Pancreatic islet transplantation is a key treatment for insulin-dependent diabetes mellitus.
  • Graft survival in islet transplantation is limited by complement activation, particularly in xenotransplantation.

Purpose of the Study:

  • To develop a method for controlling complement activation on transplanted pancreatic islets.
  • To enhance islet graft survival and enable xenoislet transplantation.

Main Methods:

  • Human soluble complement receptor 1 (sCR1) was immobilized onto islet surfaces using poly(ethylene glycol)-conjugated phospholipids (PEG-lipid).
  • Islet viability and insulin secretion function were assessed post-immobilization.

Main Results:

  • Islet cell viability and insulin secretion ability were preserved after sCR1 immobilization.
  • Immobilized sCR1 effectively inhibited complement activation on the islet surface.
  • Protected islets demonstrated resistance to attack by xenoreactive antibodies and complement.

Conclusions:

  • Surface immobilization of sCR1 on pancreatic islets is a viable strategy to prevent complement-mediated damage.
  • This approach offers a promising method to improve early islet graft survival in clinical settings.
  • The technique holds potential for enabling successful xenoislet transplantation in the future.