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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 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...
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...
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 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.
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...

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Related Experiment Video

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Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
06:27

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells

Published on: May 6, 2013

Beta-cell mass and type 1 diabetes: going, going, gone?

Eitan Akirav1, Jake A Kushner, Kevan C Herold

  • 1Department of Immunobiology, Yale University, New Haven, Connecticut, USA.

Diabetes
|October 31, 2008
PubMed
Summary

Beta-cell regeneration is key for type 1 diabetes research. Studies show residual beta-cells can be recovered or regenerate, offering therapeutic potential for diabetes treatment.

Area of Science:

  • Endocrinology
  • Immunology
  • Regenerative Medicine

Background:

  • Type 1 diabetes is characterized by beta-cell loss.
  • Beta-cell regeneration is a critical but challenging research area.
  • Understanding beta-cell dynamics is crucial for developing effective treatments.

Purpose of the Study:

  • To review recent human and animal studies on beta-cell destruction and regeneration in type 1 diabetes.
  • To explore the implications of these findings for type 1 diabetes treatment strategies.

Main Methods:

  • Review of recent human and animal studies.
  • Analysis of beta-cell destruction and regeneration processes.
  • Examination of beta-cell dynamics in nonobese diabetic (NOD) mice and humans.

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Isolation of Human Islets from Partially Pancreatectomized Patients
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Isolation of Human Islets from Partially Pancreatectomized Patients

Published on: July 30, 2011

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets
10:09

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets

Published on: May 11, 2015

Related Experiment Videos

Last Updated: Jun 28, 2026

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
06:27

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells

Published on: May 6, 2013

Isolation of Human Islets from Partially Pancreatectomized Patients
11:10

Isolation of Human Islets from Partially Pancreatectomized Patients

Published on: July 30, 2011

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets
10:09

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets

Published on: May 11, 2015

Main Results:

  • Beta-cell loss in type 1 diabetes results from destruction and regeneration.
  • Islet inflammation can stimulate beta-cell replication, but may also enhance autoimmune attack.
  • In NOD mice, high beta-cell replication occurs at diagnosis; arresting autoimmunity can lead to new beta-cell formation.
  • In humans, residual beta-cells post-treatment or during remission are often recovered, degranulated cells.

Conclusions:

  • Residual beta-cells are vital for designing therapeutic trials.
  • These cells may respond to combination therapies stimulating metabolic function.
  • Residual beta-cells represent a potential source for endogenous beta-cell regeneration.