Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
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...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Systematic Review of Interventions to Optimize Emergency Department Care of Patients with Cancer.

The western journal of emergency medicine·2026
Same author

Bringing together conceptualisations of the health advocacy competence across the continuum of medical education: a scoping review protocol.

BMJ open·2025
Same author

The global prevalence and impact of steatotic liver disease and viral infections: A systematic review and meta-analysis.

Hepatology communications·2025
Same author

Core Patient-Centered Outcomes for Adolescents and Young Adults with Cancer: A Comprehensive Review of the Literature from the STRONG-AYA Project.

Cancers·2025
Same author

Value-based healthcare from a military health system perspective: a systematic review.

BMJ open·2024
Same author

Management of Postthyroidectomy Hypoparathyroidism and Its Effect on Hypocalcemia-Related Complications: A Meta-Analysis.

Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery·2023
Same journal

The impact of avobenzone and oxybenzone on fibroblast and keratinocyte membranes. Searching for the role of lipids in the effect of UV filters on skin cells.

Chemistry and physics of lipids·2026
Same journal

Interaction of tryptophan-based peptides with mixed lipid bilayers modulates bilayers' hydrophobic region in an anionic lipid-dependent manner.

Chemistry and physics of lipids·2026
Same journal

Emerging roles of dehydrogenase/reductase (DHRS) in cancer.

Chemistry and physics of lipids·2026
Same journal

Molecular dynamics insights into lipid bilayer electroporation under constant versus pulsed DC electric fields.

Chemistry and physics of lipids·2026
Same journal

7-ketocholesterol as a theranostic target: Potential applications and future perspectives.

Chemistry and physics of lipids·2026
Same journal

Corrigendum to Lipid membrane behavior of nitro-fatty acids and their loading into liposomes to activate Nrf2 pathway in RAW264.7 cells with impact on intracellular NO production [Chem. Phys. Lipids 270 (2025) 105497].

Chemistry and physics of lipids·2026
See all related articles

Related Experiment Video

Updated: Jun 22, 2026

Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils
15:04

Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils

Published on: September 28, 2019

Membrane permeabilization by Islet Amyloid Polypeptide.

Maarten F M Engel1

  • 1Astbury Centre for Structural Molecular Biology and Institute of Molecular and Cellular Biology, University of Leeds, UK. m.engel@leeds.ac.uk

Chemistry and Physics of Lipids
|June 9, 2009
PubMed
Summary
This summary is machine-generated.

Soluble oligomers of Islet Amyloid Polypeptide (IAPP) are cytotoxic in type 2 diabetes, not insoluble fibrils. These oligomers disrupt beta-cell membranes, leading to cell death.

More Related Videos

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

Visualization of Endogenous Mitophagy Complexes In Situ in Human Pancreatic Beta Cells Utilizing Proximity Ligation Assay
08:40

Visualization of Endogenous Mitophagy Complexes In Situ in Human Pancreatic Beta Cells Utilizing Proximity Ligation Assay

Published on: May 2, 2019

Related Experiment Videos

Last Updated: Jun 22, 2026

Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils
15:04

Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils

Published on: September 28, 2019

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

Visualization of Endogenous Mitophagy Complexes In Situ in Human Pancreatic Beta Cells Utilizing Proximity Ligation Assay
08:40

Visualization of Endogenous Mitophagy Complexes In Situ in Human Pancreatic Beta Cells Utilizing Proximity Ligation Assay

Published on: May 2, 2019

Area of Science:

  • Biochemistry
  • Cell Biology
  • Endocrinology

Background:

  • Islet Amyloid Polypeptide (IAPP) aggregation is implicated in type 2 diabetes mellitus (T2DM) pathogenesis.
  • IAPP-induced cytotoxicity and beta-cell death are linked to membrane permeabilization.
  • Insoluble pancreatic IAPP deposits are not the primary cause of beta-cell membrane damage.

Purpose of the Study:

  • To review the structures and membrane interactions of various IAPP species.
  • To discuss proposed hypotheses for IAPP-induced membrane permeabilization and cytotoxicity.

Main Methods:

  • Literature review of structural and mechanistic studies on IAPP.
  • Analysis of proposed pathways for IAPP aggregation and membrane interaction.

Main Results:

  • Soluble IAPP oligomers, not insoluble fibrils, are considered cytotoxic.
  • Oligomers may induce cytotoxicity by forming membrane channels or disrupting lipid bilayers.
  • Membrane-bound, alpha-helical IAPP monomers are potential intermediates in aggregation.
  • Fibril elongation at the membrane, rather than pre-formed fibrils, may cause disruption.

Conclusions:

  • Soluble IAPP oligomers are the main culprits in beta-cell membrane permeabilization and cytotoxicity in T2DM.
  • Understanding IAPP's membrane interactions is crucial for developing T2DM therapies.