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Related Concept Videos

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...
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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.
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Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively manages...
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Related Experiment Video

Updated: May 29, 2026

Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets
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Stimulating beta cell replication and improving islet graft function by GPR119 agonists.

Jie Gao1, Lei Tian, Guobin Weng

  • 1Department of Surgery and Schulze Diabetes Institute, University of Minnesota, Minneapolis, MN, USA.

Transplant International : Official Journal of the European Society for Organ Transplantation
|September 10, 2011
PubMed
Summary

Oleoylethanolamide (OEA) and a GPR119 agonist stimulated beta-cell replication in vitro and in vivo. This approach improved islet graft function and accelerated normoglycemia in diabetic mice.

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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

Area of Science:

  • Endocrinology
  • Cell Biology
  • Pharmacology

Background:

  • G protein-coupled receptor 119 (GPR119) is expressed in pancreatic beta cells and intestinal L cells.
  • GPR119 plays a role in regulating glucose homeostasis and insulin secretion.
  • Understanding GPR119's function is crucial for developing novel diabetes therapies.

Purpose of the Study:

  • To investigate the effects of the GPR119 endogenous ligand, oleoylethanolamide (OEA), and a synthetic agonist (PSN632408) on beta-cell replication.
  • To evaluate the impact of GPR119 activation on islet graft function in a diabetic mouse model.

Main Methods:

  • In vitro studies using cultured mouse islets to assess beta-cell proliferation.
  • In vivo studies involving marginal syngeneic islet transplantation in diabetic mice.
  • Administration of OEA or PSN632408 to assess effects on normoglycemia and beta-cell replication in grafts.

Main Results:

  • OEA and PSN632408 significantly increased beta-cell replication (insulin+/5-bromo-2'-deoxyuridine (BrdU)+ cells) in cultured islets.
  • Diabetic mice treated with OEA or PSN632408 achieved normoglycemia faster post-islet transplantation compared to controls.
  • Islet grafts in OEA- or PSN632408-treated mice showed a significantly higher percentage of replicating beta cells.

Conclusions:

  • GPR119 activation by OEA or PSN632408 stimulates beta-cell replication both in vitro and in vivo.
  • Targeting GPR119 represents a promising therapeutic strategy for increasing beta-cell mass.
  • Enhancing beta-cell replication via GPR119 agonists can improve islet graft function and glycemic control.