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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...
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...
Glucose Homeostasis: Regulation of Blood Glucose01:02

Glucose Homeostasis: Regulation of Blood Glucose

Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
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...
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...
Feedback Loops01:01

Feedback Loops

In most cases, excessive hormone production is prevented by negative feedback—a loop that starts with a stimulus inducing the release of a particular substance, like a hormone, to maintain a certain level before triggering a signal that results in a decrease in further release of the hormone.

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An In Ovo Model for Testing Insulin-mimetic Compounds
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Published on: April 23, 2018

An integrated model for the glucose-insulin system.

Hanna E Silber1, Petra M Jauslin, Nicolas Frey

  • 1Department of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden. hanna.silber@novartis.com

Basic & Clinical Pharmacology & Toxicology
|January 7, 2010
PubMed
Summary

This study presents an integrated glucose-insulin model, initially for intravenous glucose tests in healthy and type 2 diabetic individuals. The model now describes oral glucose challenges, meals, and insulin administration, aiding anti-diabetic drug assessment.

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Area of Science:

  • Physiology
  • Pharmacology
  • Mathematical Modeling

Background:

  • The glucose-insulin system is crucial for metabolic homeostasis.
  • Understanding this system is vital for managing type 2 diabetes.
  • Existing models often lack comprehensive integration of glucose and insulin dynamics.

Purpose of the Study:

  • To present an integrated glucose-insulin model.
  • To demonstrate its applicability across various glucose/insulin challenge types.
  • To showcase its utility in drug development and experimental design.

Main Methods:

  • Development of a mechanism-based model for glucose and insulin.
  • Simultaneous description of glucose and insulin time-courses.
  • Extension of the model to accommodate intravenous, oral, meal, and insulin administration challenges.

Main Results:

  • The integrated model successfully describes glucose and insulin dynamics.
  • The model accommodates experiments ranging from 4 to 24 hours.
  • Applications include assessing anti-diabetic drug mechanisms and effects.

Conclusions:

  • The integrated glucose-insulin model is a versatile tool.
  • It aids in understanding glucose metabolism and insulin sensitivity.
  • The model optimizes clinical trial design and drug efficacy evaluation.