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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...
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...
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
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: Jul 7, 2026

Mechanisms Underlying Gut Hormone Secretion Using the Isolated Perfused Rat Small Intestine
07:00

Mechanisms Underlying Gut Hormone Secretion Using the Isolated Perfused Rat Small Intestine

Published on: February 26, 2019

Glucagon receptors.

F Authier1, B Desbuquois

  • 1INSERM, U756, Châtenay-Malabry, France. francois.authier@u-psud.fr

Cellular and Molecular Life Sciences : CMLS
|February 23, 2008
PubMed
Summary
This summary is machine-generated.

Glucagon receptor research has advanced, focusing on its structure, function, and gene expression. Understanding glucagon receptor mechanisms is key for metabolic homeostasis and developing new therapies.

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Mixed Primary Cultures of Murine Small Intestine Intended for the Study of Gut Hormone Secretion and Live Cell Imaging of Enteroendocrine Cells

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Related Experiment Videos

Last Updated: Jul 7, 2026

Mechanisms Underlying Gut Hormone Secretion Using the Isolated Perfused Rat Small Intestine
07:00

Mechanisms Underlying Gut Hormone Secretion Using the Isolated Perfused Rat Small Intestine

Published on: February 26, 2019

Measuring Relative Insulin Secretion using a Co-Secreted Luciferase Surrogate
05:58

Measuring Relative Insulin Secretion using a Co-Secreted Luciferase Surrogate

Published on: June 25, 2019

Mixed Primary Cultures of Murine Small Intestine Intended for the Study of Gut Hormone Secretion and Live Cell Imaging of Enteroendocrine Cells
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Mixed Primary Cultures of Murine Small Intestine Intended for the Study of Gut Hormone Secretion and Live Cell Imaging of Enteroendocrine Cells

Published on: April 20, 2017

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Biochemistry

Background:

  • Glucagon is a pancreatic hormone crucial for glucose homeostasis, acting counter to insulin.
  • The glucagon receptor (GCGR) is a G protein-coupled receptor (GPCR) involved in mediating glucagon's effects.
  • Understanding GCGR is vital for metabolic disease research.

Purpose of the Study:

  • To review current knowledge on glucagon receptor structure, function, and expression.
  • To highlight progress in identifying molecular determinants for ligand binding and signal transduction.
  • To discuss the development of glucagon analogs and receptor antagonists.

Main Methods:

  • Literature review of recent advancements in glucagon receptor research.
  • Analysis of studies on molecular determinants of ligand binding and signal transduction.
  • Examination of research on glucagon receptor gene expression regulation.

Main Results:

  • Significant progress in identifying molecular determinants of GCGR for ligand binding and signal transduction.
  • Development of glucagon analogs and small molecule receptor antagonists.
  • Characterization of mechanisms regulating glucagon receptor gene expression.

Conclusions:

  • The review consolidates current understanding of glucagon receptor structure, function, and expression.
  • Emphasis is placed on the metabolic fate of glucagon and receptor-ligand endocytosis.
  • Further research into GCGR is essential for advancing metabolic disease therapies.