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Related Concept Videos

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 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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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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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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Cells and Secretions of the Pancreas01:16

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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.
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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.
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Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells
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Slow potentials encode intercellular coupling and insulin demand in pancreatic beta cells.

Fanny Lebreton1, Antoine Pirog, Isma Belouah

  • 1CNRS UMR 5248, Chimie et Biologie des Membranes et Nano-objets, Université de Bordeaux, Batiment B14, Allée Geoffroy St Hilaire, CS90063, 33615, Pessac, France.

Diabetologia
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Summary

Researchers discovered a new electrical signal, slow potentials (SPs), in beta cells that correlate with glucose levels. These slow potentials, observed in mouse and human islets, indicate synchronized cell function and may protect against hypoglycemia.

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Area of Science:

  • Endocrinology
  • Neuroscience
  • Biophysics

Background:

  • Ion fluxes in beta cells are crucial for insulin secretion and gene regulation.
  • Understanding beta cell electrical activity is key to deciphering islet homeostasis and developing monitoring sensors.

Purpose of the Study:

  • To characterize novel electrical signals in mouse and human islets.
  • To investigate the relationship between electrical activity, glucose concentration, and hormonal regulation.
  • To explore the functional implications of observed electrical phenomena, such as hysteresis.

Main Methods:

  • Culturing mouse and human islets on multielectrode arrays (MEAs) for extended periods.
  • Recording and analyzing extracellular electrical activities, including action potentials and slow potentials (SPs).
  • Utilizing pharmacological agents and beta cell-specific knockout mice to elucidate the mechanisms underlying SP generation.

Main Results:

  • Identified two distinct extracellular voltage waveforms: action potentials and previously undescribed slow potentials (SPs).
  • Demonstrated that SP frequency correlates directly with glucose concentration, peaking at 10 mmol/l, and is augmented by GLP-1.
  • Confirmed SPs are mediated by ATP-dependent potassium channels and cell coupling via connexin 36, exhibiting hysteresis with glucose ramps.

Conclusions:

  • Introduced a novel electrical signature (SPs) reflecting the syncytial function and beta cell specificity of islets.
  • Provided evidence that observed hysteresis in SPs represents an endogenous protective mechanism against hypoglycemia.