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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...
Tissue Renewal without Stem Cells01:23

Tissue Renewal without Stem Cells

After cellular or tissue damage, the resident stem cells present in the human body can locally repair and regenerate the damaged tissue or organ. However, even though some tissues do not have stem cells, they can repair and regenerate with the help of pre-existing cells. For example, beta cells of the pancreas and hepatocytes of the liver can divide to renew and regenerate the tissue. Here, both cell division and cell death are well regulated by homeostasis.
However, failure of such a system...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

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 co-secreted in...
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.
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

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...
Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...

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Related Experiment Video

Updated: Jul 6, 2026

Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets
09:31

Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets

Published on: June 25, 2012

Preservation of beta-cell function by targeting beta-cell mass.

Eelco J P de Koning1, Susan Bonner-Weir, Ton J Rabelink

  • 1Department of Nephrology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands. e.dekoning@lumc.nl <e.dekoning@lumc.nl>

Trends in Pharmacological Sciences
|March 25, 2008
PubMed
Summary

Type 2 diabetes involves progressive beta-cell loss. New therapies targeting glucagon-like peptide-1 and growth factors offer promising strategies for preserving and expanding beta-cell mass to manage blood sugar.

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Sustained Administration of &#946;-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres
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High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
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High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds

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Last Updated: Jul 6, 2026

Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets
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Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets

Published on: June 25, 2012

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

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High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
12:32

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds

Published on: January 23, 2018

Area of Science:

  • Endocrinology and Metabolism
  • Cell Biology
  • Pharmacology

Background:

  • Type 2 diabetes is marked by declining pancreatic beta-cell function and mass.
  • High glucose, inflammatory cytokines, and free fatty acids induce beta-cell apoptosis.
  • Reduced beta-cell mass compromises the body's ability to maintain normal blood glucose levels.

Purpose of the Study:

  • To review mechanisms underlying beta-cell dysfunction and loss in type 2 diabetes.
  • To explore therapeutic strategies for preserving and expanding beta-cell mass.
  • To provide a rationale for pharmacological interventions in type 2 diabetes management.

Main Methods:

  • Review of existing literature on beta-cell biology and type 2 diabetes.
  • Analysis of mechanisms contributing to beta-cell dysfunction and apoptosis.
  • Evaluation of emerging therapeutic approaches for beta-cell preservation.

Main Results:

  • Beta-cell mass reduction is a key feature of type 2 diabetes progression.
  • Adverse factors like hyperglycemia and lipotoxicity accelerate beta-cell loss.
  • Glucagon-like peptide-1 based therapies and growth factor combinations show potential for beta-cell regeneration.

Conclusions:

  • Preserving or expanding beta-cell mass is crucial for achieving normoglycemia in type 2 diabetes.
  • Pharmacological interventions targeting specific pathways offer a viable strategy.
  • Further research into novel therapies is warranted to combat beta-cell loss.