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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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After cellular or tissue damage, the resident stem cells present in the human body can locally repair and regenerate the damaged tissue or organ. However, even though some tissues do not have stem cells, they can repair and regenerate with the help of pre-existing cells. For example, beta cells of the pancreas and hepatocytes of the liver can divide to renew and regenerate the tissue. Here, both cell division and cell death are well regulated by homeostasis.
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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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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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Insulin: Biosynthesis, Chemistry, and Preparation01:25

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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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Nutrients men-TOR β-Cells to Adulthood.

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In fetuses, amino acids activate mTOR to trigger insulin secretion, unlike adults where glucose is the main trigger. Reducing amino acids aids the maturation of stem cell-derived beta cells.

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Area of Science:

  • Endocrinology
  • Developmental Biology
  • Metabolism

Background:

  • Glucose is the primary stimulator of insulin secretion in adult pancreatic beta cells.
  • Understanding fetal beta cell development and insulin secretion regulation is crucial for regenerative medicine and treating diabetes.

Purpose of the Study:

  • To investigate the key regulators of insulin secretion in fetal pancreatic beta cells.
  • To explore the role of amino acids and mTOR signaling in fetal beta cell function.
  • To determine if manipulating amino acid levels can enhance the maturation of stem cell-derived beta cells.

Main Methods:

  • Utilized pluripotent stem cells differentiated into pancreatic beta cells.
  • Analyzed insulin secretion in response to various stimuli, including amino acids and glucose.
  • Investigated the involvement of the mechanistic target of rapamycin (mTOR) pathway.

Main Results:

  • Fetal beta cells primarily rely on amino acid activation of mTOR for insulin secretion.
  • Reducing amino acid availability promoted the maturation of pluripotent stem cell-derived beta cells.
  • Distinct regulatory mechanisms govern insulin secretion in fetal versus adult beta cells.

Conclusions:

  • Amino acid-mTOR signaling is a critical regulator of fetal beta cell insulin secretion.
  • Targeting amino acid metabolism presents a potential strategy for improving beta cell maturation from stem cells.
  • This study reveals key developmental differences in beta cell function, offering insights into diabetes research.