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

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
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 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...
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...
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...

You might also read

Related Articles

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

Sort by
Same author

Molecular mechanisms associated with breast cancer based on integrated gene expression profiling by bioinformatics analysis.

Journal of obstetrics and gynaecology : the journal of the Institute of Obstetrics and Gynaecology·2016
Same author

Visceral fat dysfunction is positively associated with hypogonadism in Chinese men.

Scientific reports·2016
Same author

Fingerprint Analysis of Desmodium Triquetrum L. Based on Ultra Performance Liquid Chromatography with Photodiode Array Detector Combined with Chemometrics Methods.

Journal of chromatographic science·2016
Same author

Neck circumference as an independent indicator to non-alcoholic fatty liver disease in non-obese men.

Nutrition & metabolism·2016
Same author

Associations between implementation characteristics and evidence-based practice sustainment: a study of the Adolescent Community Reinforcement Approach.

Implementation science : IS·2015
Same author

A pre-post pilot study of peer nutritional counseling and food insecurity and nutritional outcomes among antiretroviral therapy patients in Honduras.

BMC nutrition·2015
Same journal

The scaffolding protein AKAP79/150 shapes innate immune responses to allergen.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same journal

Optineurin restrains IL-17-associated neuroinflammation in trigeminal ganglia to preserve sensory function after ocular HSV-1 infection.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same journal

Crystal structure and immune single-cell atlas provide insights into the functional divergence of type I IFNs in fish.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same journal

Complement C3 deficiency increases the effector and cytotoxic functions of NK cells and suppresses tumor growth.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same journal

Increased Nur77 is disconnected from TCR affinity in insulin-specific Tregs.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same journal

FTR85 negatively regulates type I IFN antiviral signaling pathway by promoting K48-linked polyubiquitination of IRF3.

Journal of immunology (Baltimore, Md. : 1950)·2026
See all related articles

Related Experiment Video

Updated: Jun 3, 2026

Sustained Administration of β-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

TGF-beta i promotes islet beta-cell function and regeneration.

Bing Han1, Shijie Qi, Bing Hu

  • 1Laboratoire Immunologie, Centre de Recherche, Centre Hospitalier de l'Université de Montréal-Hôpital Notre-Dame, Montréal, Quebec H2L 4M1, Canada.

Journal of Immunology (Baltimore, Md. : 1950)
|April 8, 2011
PubMed
Summary
This summary is machine-generated.

Transforming growth factor-beta induced protein (TGF-βi) significantly enhances islet cell survival and function. This vital trophic factor promotes islet regeneration and improves glucose tolerance in mice.

More Related Videos

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform
09:35

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

Published on: July 16, 2016

Optimized Protocol for Generating Functional Pancreatic Insulin-secreting Cells from Human Pluripotent Stem Cells
06:33

Optimized Protocol for Generating Functional Pancreatic Insulin-secreting Cells from Human Pluripotent Stem Cells

Published on: February 2, 2024

Related Experiment Videos

Last Updated: Jun 3, 2026

Sustained Administration of β-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

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform
09:35

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

Published on: July 16, 2016

Optimized Protocol for Generating Functional Pancreatic Insulin-secreting Cells from Human Pluripotent Stem Cells
06:33

Optimized Protocol for Generating Functional Pancreatic Insulin-secreting Cells from Human Pluripotent Stem Cells

Published on: February 2, 2024

Area of Science:

  • Endocrinology
  • Cell Biology
  • Molecular Biology

Background:

  • Transforming growth factor-beta induced protein (TGF-βi) is a bifunctional molecule that enhances extracellular matrix (ECM) and cell interactions.
  • Dysfunction in ECM-cell interactions can lead to impaired cell function.
  • The role of TGF-βi in pancreatic islet biology was previously unclear.

Purpose of the Study:

  • To investigate the role of TGF-βi in the function and survival of pancreatic islets.
  • To elucidate the signaling pathways involved in TGF-βi's effects on islets.

Main Methods:

  • DNA microarray and quantitative PCR to assess TGFβi gene expression in cultured islets.
  • Administration of recombinant TGF-βi to cultured islets and assessment of islet function and integrity.
  • FAK knockdown using small interfering RNA (siRNA) in islets.
  • Analysis of TGF-βi transgenic (Tg) mouse pancreata and islets in vitro and in vivo.
  • Glucose tolerance tests in Tg and wild-type mice.
  • Transplantation of Tg islets into diabetic mice.

Main Results:

  • TGFβi gene expression significantly increased in cultured islets.
  • Recombinant TGF-βi preserved islet integrity and enhanced function, mediated by Focal Adhesion Kinase (FAK) signaling.
  • FAK knockdown impaired islet function.
  • Tg islets exhibited improved integrity, insulin release, and β-cell proliferation.
  • Tg mice showed enhanced glucose tolerance and transplanted Tg islets demonstrated potent blood glucose-lowering capacity and regeneration.

Conclusions:

  • TGF-βi acts as a crucial trophic factor for islet survival, function, and regeneration.
  • TGF-βi signaling, at least partly through FAK, mediates these beneficial effects on islets.
  • TGF-βi holds potential for therapeutic strategies targeting diabetes and islet dysfunction.