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

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 II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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...
Carbohydrate Metabolism01:36

Carbohydrate Metabolism

Carbohydrates are polymers composed of molecules containing atoms of carbon, hydrogen and oxygen. One gram of carbohydrate can provide four kilo-calories of energy, which makes it the most efficient instant energy source.
Starch accounts for approximately 60% of the carbohydrates consumed by humans. Since amylase enzymes cannot function in the stomach's acidic environment, starch can only be digested in the mouth and small intestine. Simple sugars are found naturally in milk and fruits in the...
Diabetes Mellitus: Overview and Type I Subtype01:22

Diabetes Mellitus: Overview and Type I Subtype

Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...

You might also read

Related Articles

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

Sort by
Same author

Postpartum screening for type 2 diabetes mellitus in women with gestational diabetes: Is it really performed?

Diabetes research and clinical practice·2020
Same author

The role of adipokines in the pathogenesis of gestational diabetes mellitus.

Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology·2019
Same author

Early vs. standard screening and treatment of gestational diabetes in high-risk women - An attempt to determine relative advantages and disadvantages.

Nutrition, metabolism, and cardiovascular diseases : NMCD·2019
Same author

The use of real time continuous glucose monitoring or flash glucose monitoring in the management of diabetes: A consensus view of Italian diabetes experts using the Delphi method.

Nutrition, metabolism, and cardiovascular diseases : NMCD·2019
Same author

Thermal treatment reduces gliadin recognition by IgE, but a subsequent digestion and epithelial crossing permits recovery.

Food research international (Ottawa, Ont.)·2019
Same author

Factors influencing safe glucose-lowering in older adults with type 2 diabetes: A PeRsOn-centred ApproaCh To IndiVidualisEd (PROACTIVE) Glycemic Goals for older people: A position statement of Primary Care Diabetes Europe.

Primary care diabetes·2019

Related Experiment Video

Updated: Jul 3, 2026

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

Beta-cell apoptosis in type 2 diabetes: quantitative and functional consequences.

R Lupi1, S Del Prato

  • 1Department of Endocrinology and Metabolism, Section of Diabetes and Metabolic Diseases, University of Pise, Italy.

Diabetes & Metabolism
|July 22, 2008
PubMed
Summary

Type 2 diabetes involves reduced beta-cell function and mass, primarily due to increased apoptosis. Understanding these mechanisms is key to developing new therapies for insulin deficiency.

More Related Videos

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
12:12

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Published on: June 16, 2011

Measurement of Differentially Methylated INS DNA Species in Human Serum Samples as a Biomarker of Islet β Cell Death
10:34

Measurement of Differentially Methylated INS DNA Species in Human Serum Samples as a Biomarker of Islet β Cell Death

Published on: December 21, 2016

Related Experiment Videos

Last Updated: Jul 3, 2026

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
12:12

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Published on: June 16, 2011

Measurement of Differentially Methylated INS DNA Species in Human Serum Samples as a Biomarker of Islet β Cell Death
10:34

Measurement of Differentially Methylated INS DNA Species in Human Serum Samples as a Biomarker of Islet β Cell Death

Published on: December 21, 2016

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Cell Biology

Background:

  • Type 2 diabetes is the most common form of diabetes.
  • It is characterized by insulin resistance and impaired insulin secretion.
  • A reduction in pancreatic beta-cell mass is observed in type 2 diabetes.

Purpose of the Study:

  • To discuss the mechanisms of beta-cell loss in type 2 diabetes.
  • To explore potential therapeutic strategies for preventing beta-cell death.
  • To maintain beta-cell mass and function in type 2 diabetes.

Main Methods:

  • Review of existing literature on beta-cell apoptosis in type 2 diabetes.
  • Analysis of molecular mechanisms underlying beta-cell loss.
  • Discussion of emerging therapeutic targets for beta-cell preservation.

Main Results:

  • Pancreatic beta-cell apoptosis plays a critical role in insulin deficiency.
  • The balance between beta-cell replication and apoptosis is crucial for maintaining mass.
  • Several molecular pathways contribute to increased beta-cell death in type 2 diabetes.

Conclusions:

  • Targeting apoptosis pathways offers a promising therapeutic approach.
  • Preserving beta-cell mass is essential for managing type 2 diabetes.
  • Further research into novel therapeutic strategies is warranted.