Related Experiment Video

Updated: Jul 15, 2026

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
12:33

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination

Published on: June 25, 2014

Therapeutic approaches to preserve islet mass in type 2 diabetes

Laurie L Baggio1, Daniel J Drucker

  • 1Department of Medicine, Toronto General Hospital, Banting and Best Diabetes Center, University of Toronto, Toronto, Ontario, Canada M5S 2S2.

Annual Review of Medicine
|January 18, 2006
PubMed

Insights

Type 2 diabetes treatments like GLP-1 agonists and DPP-IV inhibitors can increase beta-cell mass. These therapies, alongside others, show potential to reverse beta-cell loss in type 2 diabetes.

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Pharmacology

Background:

  • Type 2 diabetes involves hyperglycemia due to insulin resistance and insufficient beta-cell function.
  • Current treatments lower blood glucose but do not restore beta-cell mass.
  • Declining beta-cell mass is a hallmark of type 2 diabetes progression.

Purpose of the Study:

  • To review therapeutic strategies that may reverse the decline in beta-cell mass in type 2 diabetes.
  • To explore mechanisms by which agents like GLP-1 receptor agonists, GIP receptor agonists, and DPP-IV inhibitors impact beta-cell mass.
  • To assess the potential of combination therapies for beta-cell regeneration.

Main Methods:

  • Review of preclinical data on therapeutic agents affecting beta-cell mass.
  • Analysis of signaling pathways involved in beta-cell replication and apoptosis.
  • Examination of agents including GLP-1 receptor agonists, GIP receptor activation, DPP-IV inhibitors, and thiazolidinediones (TZDs).

Main Results:

  • GLP-1 receptor agonists stimulate beta-cell replication and inhibit apoptosis.
  • GIP receptor activation enhances insulin secretion, proliferation, and reduces apoptosis.
  • DPP-IV inhibition and TZDs also contribute to preserving or expanding beta-cell mass.
  • Combination therapies, like epidermal growth factor and gastrin, promote islet neogenesis in rodent models.

Conclusions:

  • Several therapeutic approaches, including GLP-1 and GIP pathway modulation, show promise in expanding beta-cell mass.
  • These strategies may offer a way to counteract the natural decline of beta-cell mass in type 2 diabetes.
  • Combination therapies represent a potential avenue for more effective beta-cell regeneration.

More Related Videos

Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres09:31

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

Scaffold-supported Transplantation of Islets in the Epididymal Fat Pad of Diabetic Mice11:57

Scaffold-supported Transplantation of Islets in the Epididymal Fat Pad of Diabetic Mice

Published on: July 23, 2017

Related Concept Videos

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...
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...
Diabetes: Management and Pharmacotherapy01:15

Diabetes: Management and Pharmacotherapy

The therapy for diabetes aims to alleviate hyperglycemia-related symptoms, prevent acute metabolic decompensation, and reduce chronic end-organ complications. Glycemic control is evaluated through short-term (self-monitoring, continuous glucose monitoring) and long-term (A1c, fructosamine) metrics, enabling near real-time tracking of blood glucose levels and reflecting glycemic control over specific time frames.
Insulin remains the cornerstone of treatment for most patients with type 1 and many...
Insulin: Dosing Regimen and Adverse Effects01:16

Insulin: Dosing Regimen and Adverse Effects

Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
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...