Related Experiment Video

Updated: May 15, 2026

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

Dual effect of advanced glycation end products in pancreatic islet apoptosis

Flavia Costal1, Erika Oliveira, Alexandre Raposo

  • 1Faculdade de Medicina da Universidade de São Paulo, Laboratório de Endocrinologia Celular e Molecular LIM-25, São Paulo, Brazil.

Diabetes/Metabolism Research and Reviews
|January 15, 2013
PubMed
Abstract

Insights

Advanced glycation end products (AGEs) show a dual effect on pancreatic islets. Short exposure protects against apoptosis, while prolonged exposure promotes islet cell death, impacting type 2 diabetes.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Diabetes Research

Background:

  • Type 2 diabetes is characterized by loss of β-cell function, impacting metabolic control.
  • Advanced glycation end products (AGEs) and their receptors (RAGE) contribute to islet apoptosis, alongside amyloid deposits and glucolipotoxicity.
  • Investigating the specific role of AGEs in β-cell deterioration is crucial for understanding diabetes progression.

Purpose of the Study:

  • To evaluate the temporal and dose-dependent effects of AGE compounds on apoptosis rate in cultured islets.
  • To assess the impact of AGEs on reactive oxygen species generation and gene expression related to apoptosis.
  • To elucidate the mechanism of AGE-induced β-cell dysfunction.

Main Methods:

  • Rat pancreatic islets were exposed to AGE-modified albumin for 24, 48, 72, and 96 hours.
  • Apoptosis, reactive oxygen species (ROS), superoxide content, and NADPH oxidase activity were measured.
  • RNA expression of RAGE (Ager), Bax, Bcl2, and Nfkb1 genes was analyzed.

Main Results:

  • Short-term AGE exposure (24-48h) decreased apoptosis, reduced the Bax/Bcl2 ratio, and lowered Nfkb1 expression.
  • Prolonged AGE exposure (72-96h) increased apoptosis, elevated the Bax/Bcl2 ratio, and upregulated Nfkb1 expression.
  • AGEs initially decreased ROS but later increased superoxide generation, with NADPH oxidase implicated in ROS production.

Conclusions:

  • Albumin modified by glycoaldehyde exhibits a dual effect on cultured pancreatic islets.
  • Short-term AGE exposure demonstrates a protective role against apoptosis.
  • Prolonged AGE exposure promotes apoptosis, contributing to β-cell deterioration in type 2 diabetes.

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

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform09:35

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

Published on: July 16, 2016

Related Concept Videos

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 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...
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.
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Cells and Secretions of the Pancreas01:16

Cells and Secretions of the Pancreas

The pancreas, a vital organ within the abdominal cavity, plays dual roles in the digestive and endocrine systems, collaborating with exocrine and endocrine cells to maintain optimal digestion and blood sugar levels.
Exocrine function is carried out by acinar cells, organized into clusters known as acini. These cells contribute to digestion by releasing substantial quantities of enzyme-rich, alkaline digestive juices.
Concurrently, the dispersed clusters of endocrine cells throughout the...
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...