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Related Concept Videos

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

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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...
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Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

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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.
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Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

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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...
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Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

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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...
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Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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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...
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Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
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Related Experiment Video

Updated: Apr 25, 2026

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
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A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination

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Reversible changes in pancreatic islet structure and function produced by elevated blood glucose.

Melissa F Brereton1, Michaela Iberl2, Kenju Shimomura2

  • 1Henry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics and OXION, University of Oxford, Parks Road, Oxford OX1 3PT, UK.

Nature Communications
|August 23, 2014
PubMed
Summary

High blood sugar (hyperglycaemia) alone causes many diabetes-related changes in pancreatic islet cells. These alterations in insulin and glucagon cells are reversible with blood glucose normalization.

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Area of Science:

  • Endocrinology
  • Metabolic diseases
  • Cell biology

Background:

  • Diabetes mellitus involves impaired insulin and glucagon secretion due to pancreatic islet dysfunction.
  • The specific role of hyperglycaemia in causing these islet cell changes is not fully understood.

Purpose of the Study:

  • To investigate whether hyperglycaemia per se drives alterations in pancreatic islet cell function and morphology.
  • To determine if these hyperglycaemia-induced changes are reversible.

Main Methods:

  • Induction of a human activating KATP channel mutation in adult mice to cause rapid diabetes and hyperglycaemia.
  • Analysis of islet morphology, cell types (insulin-positive beta-cells, glucagon-positive alpha-cells), and gene expression.
  • Assessment of the effects of insulin therapy and sulphonylureas on islet alterations.

Main Results:

  • Activating KATP channel mutation in mice rapidly induced diabetes with significant islet structural and functional changes.
  • Chronic hyperglycaemia led to a decrease in insulin-positive cells and an increase in glucagon-positive cells without affecting cell turnover.
  • Some beta-cells began expressing glucagon while retaining beta-cell characteristics.
  • These changes were prevented by insulin therapy and reversed by sulphonylureas, indicating hyperglycaemia as the primary driver.

Conclusions:

  • Hyperglycaemia, not KATP channel activation, is the main cause of observed islet cell alterations in this model of diabetes.
  • The structural and functional changes in pancreatic islets associated with diabetes are largely reversible upon normalization of blood glucose levels.