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Related Concept Videos

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...
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.
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...

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

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Published on: July 16, 2016

Relationship between beta-cell mass and diabetes onset.

A V Matveyenko1, P C Butler

  • 1Larry Hillblom Islet Research Center, UCLA David Geffen School of Medicine, Los Angeles, CA 90095-7073, USA. amatveyenko@mednet.ucla.edu

Diabetes, Obesity & Metabolism
|October 18, 2008
PubMed
Summary

Diabetes progression involves beta-cell loss and dysfunction. Impaired beta-cell mass and function contribute to glucose dysregulation in type 1 and type 2 diabetes, with apoptosis playing a key role.

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Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Cell Biology

Background:

  • Adequate beta-cell mass and function are crucial for blood glucose regulation.
  • Current inability to measure human beta-cell mass in vivo necessitates reliance on autopsy studies, which can be confounded by pre- and postmortem changes.
  • Autopsy studies reveal significant beta-cell mass deficits (0-65% in T2DM, 70-100% in T1DM) and increased apoptosis in both diabetes types.

Purpose of the Study:

  • To postulate a phased model for diabetes progression.
  • To explore the roles of beta-cell cytotoxicity, apoptosis, dysfunction, and mass loss in diabetes.
  • To address the controversy regarding the relative contributions of beta-cell loss versus dysfunction to diabetes onset.

Main Methods:

  • Review and synthesis of existing autopsy and animal study data on beta-cell mass and function in diabetes.
  • Postulation of a three-phase model for diabetes progression based on beta-cell changes.
  • Analysis of the interplay between beta-cell cytotoxicity, apoptosis, and function.

Main Results:

  • A proposed three-phase model for diabetes progression: 1) selective beta-cell cytotoxicity leading to impaired function and mass loss; 2) decompensation of glucose control due to impaired insulin secretion; 3) glucose toxicity accelerating dysfunction and insulin resistance.
  • Animal studies indicate that a ~50% deficit in beta-cell mass impairs insulin secretion and induces insulin resistance.
  • Increased beta-cell apoptosis is observed in both type 1 and type 2 diabetes.

Conclusions:

  • Beta-cell loss and dysfunction are intrinsically linked processes in diabetes development.
  • Cytotoxicity leading to apoptosis inevitably impairs beta-cell function, making it difficult to isolate their independent contributions to diabetes onset.
  • Understanding these mechanisms is critical for developing effective diabetes therapies.