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.
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...
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...
Diabetes Mellitus: Type 2 and Gestational01:22

Diabetes Mellitus: Type 2 and Gestational

Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
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

Screening for CKD in undiagnosed populations with diabetes and hypertension: lessons from the SEARCH study.

Jornal brasileiro de nefrologia·2026
Same author

GLP-1 Agonist to Treat Obesity and Prevent Cardiovascular Disease: What Have We Achieved so Far?

Current atherosclerosis reports·2022
Same author

Interplay Between Thyroid Hormone Status and Pulmonary Hypertension in Graves' Disease: Relevance of the Assessment in Thyrotoxic and Euthyroid Patients.

Frontiers in endocrinology·2022
Same author

Fixed 30 mCi (1110 MBq) <sup>131</sup>I-iodine therapy in autonomously functioning nodules: Single toxic nodule as a predictive factor of success.

World journal of nuclear medicine·2022
Same author

Efficacy and safety of evogliptin in the treatment of type 2 diabetes mellitus in a Brazilian population: a randomized bridging study.

Diabetology & metabolic syndrome·2020
Same author

Updated Cardiovascular Prevention Guideline of the Brazilian Society of Cardiology - 2019.

Arquivos brasileiros de cardiologia·2019

Related Experiment Video

Updated: May 16, 2026

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

Can we prevent beta cell apoptosis in type 2 diabetes?

Freddy Goldberg Eliaschewitz1, Marcos Antonio Tambascia

  • 1Freddy Goldberg Eliaschewitz, Hospital Albert Einstein, São Paulo, Brazil; CPClin Clinical Research Center, São Paulo, Brazil, CEP-01244-030. freddy.g@uol.com.br.

Diabetes/Metabolism Research and Reviews
|December 11, 2012
PubMed
Summary

Type 2 diabetes (DM2) progression causes long-term glycemic control failure due to declining beta-cell insulin secretion. Treatment adjustments are necessary as the disease advances, as highlighted by the UKPDS study.

More Related Videos

A High-content In Vitro Pancreatic Islet &#946;-cell Replication Discovery Platform
09:35

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

Published on: July 16, 2016

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

Related Experiment Videos

Last Updated: May 16, 2026

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

A High-content In Vitro Pancreatic Islet &#946;-cell Replication Discovery Platform
09:35

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

Published on: July 16, 2016

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

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Diabetes Research

Background:

  • The United Kingdom Prospective Diabetes Study (UKPDS) identified the progressive nature of type 2 diabetes (DM2) as a primary reason for failing to achieve long-term glycemic control.
  • This progression is characterized by a continuous decline in beta-cell function, leading to insulin deficiency.

Purpose of the Study:

  • To underscore the importance of understanding the progressive nature of type 2 diabetes.
  • To highlight the necessity of adaptive treatment strategies in managing long-term glycemic control.

Main Methods:

  • Analysis of data and findings from the United Kingdom Prospective Diabetes Study (UKPDS).
  • Review of established knowledge regarding beta-cell function decline in type 2 diabetes.

Main Results:

  • Type 2 diabetes progression involves an annual reduction of approximately 5% in beta-cell insulin secretion capacity.
  • Significant beta-cell function loss (around 50%) precedes the clinical diagnosis of diabetes.
  • This decline in function begins 10-12 years prior to diagnosis.

Conclusions:

  • The progressive decline in beta-cell function is a fundamental aspect of type 2 diabetes pathophysiology.
  • Effective long-term management of type 2 diabetes requires treatment regimens that account for disease progression and declining beta-cell function.