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Related Concept Videos

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.
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Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

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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.
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Insulin: The Receptor and Signaling Pathways01:28

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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

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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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Glucose Homeostasis: Regulation of Blood Glucose01:02

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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.
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cAMP-dependent Protein Kinase Pathways01:25

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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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Analysis of Beta-cell Function Using Single-cell Resolution Calcium Imaging in Zebrafish Islets
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Newer perspective on the coupling between glucose-mediated signaling and β-cell functionality.

Jun Shirakawa1, Yasuo Terauchi1

  • 1Department of Endocrinology and Metabolism, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Endocrine Journal
|November 8, 2019
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Glucokinase, the glucose sensor in pancreatic beta-cells, regulates insulin secretion, proliferation, and survival. Understanding its signaling pathways offers new therapeutic strategies for beta-cell dysfunction.

Keywords:
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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Pancreatic beta-cells secrete insulin in response to glucose, a process vital for glucose homeostasis.
  • Glucose signaling influences beta-cell proliferation and survival, but underlying mechanisms are not fully understood.
  • Glucokinase (GCK) functions as the primary glucose sensor in beta-cells, catalyzing glucose phosphorylation.

Purpose of the Study:

  • To elucidate the molecular mechanisms of glucose signaling in beta-cell function, focusing on glucokinase.
  • To investigate the role of glucokinase in insulin secretion, beta-cell proliferation, and apoptosis.

Main Methods:

  • Utilized beta-cell-specific glucokinase-haploinsufficient (Gck+/-) mice.
  • Employed allosteric glucokinase activators (GKAs).
  • Analyzed gene expression and protein interactions related to glucose metabolism and beta-cell function.

Main Results:

  • Glucokinase-mediated metabolism suppresses ER stress-induced apoptosis by upregulating IRS-2 and ER stress markers.
  • Glucokinase promotes beta-cell proliferation via the FoxM1/PLK1/CENP-A pathway.
  • Glucokinase induces islet inflammation and alters extracellular matrix protein expression (Fbln5).

Conclusions:

  • Glucokinase plays a multifaceted role in beta-cell function, impacting apoptosis, proliferation, inflammation, and extracellular matrix regulation.
  • GLP-1 receptor agonists and DPP-4 inhibitors may offer therapeutic benefits by compensating for glucokinase dysregulation.
  • Further research into glucose/glucokinase signaling pathways is crucial for developing novel treatments for beta-cell dysfunction.