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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...
Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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...
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...
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: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
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.

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Related Experiment Video

Updated: Jun 7, 2026

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells
05:51

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells

Published on: June 15, 2013

Functional interactions between pancreatic beta cells and (pre)adipocytes.

Valerie Christiaens1, Rebecca Sujatha, Karine H Hellemans

  • 1Center for Molecular and Vascular Biology, KU Leuven, Campus Gasthuisberg, Leuven, Belgium.

Endocrine
|October 21, 2010
PubMed
Summary
This summary is machine-generated.

Pancreatic beta cells secrete insulin, promoting adipocyte differentiation. While adipocytes influence beta cells, these effects are reversible and do not cause lasting damage in this study.

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Last Updated: Jun 7, 2026

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells
05:51

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells

Published on: June 15, 2013

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

Published on: June 25, 2012

Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry
05:38

Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry

Published on: January 28, 2017

Area of Science:

  • Cell biology
  • Endocrinology
  • Metabolic disease research

Background:

  • Type 2 diabetes is linked to obesity and pancreatic beta cell dysfunction.
  • The direct interaction between adipocytes and beta cells and its pathological significance remain unclear.

Purpose of the Study:

  • To investigate the functional interactions between 3T3-F442A (pre)adipocytes and primary rat pancreatic beta cells during co-culture.
  • To determine if these interactions have pathogenic relevance for beta cell function.

Main Methods:

  • Co-culturing 3T3-F442A (pre)adipocytes with primary rat pancreatic beta cells for 9 days.
  • Assessing changes in adipocyte differentiation markers, adiponectin release, glucose consumption, and beta cell insulin secretion and degranulation.
  • Evaluating the effects of varying glucose concentrations and conditioned media.

Main Results:

  • Beta cells induced 3T3-F442A cells to differentiate into lipid-storing adipocytes, releasing adiponectin, mediated by insulin.
  • Reduced glucose levels due to adipocyte uptake suppressed beta cell insulin release and degranulation at 10 mM glucose.
  • These effects were reversible upon cell separation and did not occur at 20 mM glucose.

Conclusions:

  • Beta cell-secreted insulin is sufficient to induce preadipocyte differentiation.
  • (Pre)adipocytes do not directly or irreversibly impair beta cell function within the 9-day co-culture period.
  • The observed interactions highlight a dynamic interplay influenced by glucose and insulin levels.