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Related Concept Videos

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

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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.
Insulin and C-peptide are...
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Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

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

Insulin: The Receptor and Signaling Pathways

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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...
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Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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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...
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Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

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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...
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Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

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The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
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Related Experiment Video

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Homogeneous Time-resolved F&#246;rster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
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β Cell GHS-R Regulates Insulin Secretion and Sensitivity.

Geetali Pradhan1,2, Chia-Shan Wu3, Daniel Villarreal3

  • 1USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA.

International Journal of Molecular Sciences
|April 30, 2021
PubMed
Summary
This summary is machine-generated.

Growth hormone secretagogue receptor (GHS-R) is expressed in pancreatic cells and regulates glucose homeostasis. Blocking GHS-R in beta cells improves insulin sensitivity, suggesting potential for Type 2 Diabetes treatment.

Keywords:
MIP-Cre/ERTglucose-stimulated insulin secretion (GSIS)growth hormone secretagogue receptor (GHS-R)insulin secretioninsulin sensitivitypancreatic isletsβ cells

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Area of Science:

  • Endocrinology
  • Metabolism
  • Molecular Biology

Background:

  • The growth hormone secretagogue receptor (GHS-R) is known for regulating food intake and adiposity.
  • Its precise role in glucose homeostasis and pancreatic islet function remains largely unclear.

Purpose of the Study:

  • To investigate GHS-R expression in mouse pancreatic islets.
  • To elucidate the function of GHS-R in glycemic regulation and insulin secretion.

Main Methods:

  • Utilized Ghsr-IRES-tauGFP mice to visualize GHS-R expression via Green Fluorescent Protein (GFP) co-localization with insulin and glucagon.
  • Generated β-cell-specific GHSR-deleted mice (MIP-Cre/ERT;Ghsrf/f) to assess the impact of GHS-R deletion on glucose metabolism.
  • Performed glucose tolerance tests (GTT), glucose-stimulated insulin secretion (GSIS) tests in vivo and ex vivo, and insulin tolerance tests (ITT).

Main Results:

  • Confirmed GHS-R expression in pancreatic β and α cells.
  • Mice lacking GHS-R in β cells (MIP-Cre/ERT;Ghsrf/f) exhibited normal energy homeostasis but displayed significant alterations in glucose metabolism.
  • These mice showed lower fasting glucose and insulin levels, reduced insulin secretion in response to glucose, and improved insulin sensitivity.
  • GHS-R was found to cell-autonomously regulate glucose-stimulated insulin secretion and modulate systemic insulin sensitivity.

Conclusions:

  • β cell GHS-R plays a critical role in regulating glucose homeostasis.
  • GHS-R antagonists represent a potential therapeutic strategy for managing Type 2 Diabetes.