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Cells and Secretions of the Pancreas01:16

Cells and Secretions of the Pancreas

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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.
Exocrine function is carried out by acinar cells, organized into clusters known as acini. These cells contribute to digestion by releasing substantial quantities of enzyme-rich, alkaline digestive juices.
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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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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 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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Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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Updated: Feb 16, 2026

Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry
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Pancreatic Pericytes Support β-Cell Function in a Tcf7l2-Dependent Manner.

Lina Sakhneny1, Eleonor Rachi1, Alona Epshtein1

  • 1Department of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

Diabetes
|December 17, 2017
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Genetic variations in TCF7L2 impact pancreatic pericytes, affecting beta-cell function and glucose regulation. This study reveals TCF7L2’s role in pericytes for maintaining beta-cell health and insulin secretion, offering insights into type 2 diabetes.

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Genetics

Background:

  • Polymorphism in TCF7L2 is linked to type 2 diabetes, but the underlying mechanism involving beta-cell dysfunction is unclear.
  • Beta-cell function is influenced by their microenvironment, including pancreatic pericytes.

Purpose of the Study:

  • To investigate the role of Tcf7l2 in pancreatic pericytes for beta-cell function.
  • To elucidate the cellular and molecular mechanisms by which pericytic Tcf7l2 influences glucose homeostasis.

Main Methods:

  • Utilized transgenic mice with selective Tcf7l2 inactivation in pancreatic pericytes.
  • Assessed glucose tolerance, beta-cell function, and insulin secretion.
  • Analyzed gene expression in isolated islets and identified secreted factors from pericytes.

Main Results:

  • Selective inactivation of Tcf7l2 in pancreatic pericytes led to impaired glucose tolerance and compromised beta-cell function.
  • Pericytic Tcf7l2 deficiency altered gene expression related to beta-cell function and maturity.
  • Identified TCF7L2-dependent secretion of bone morphogenetic protein 4 (BMP4) by pericytes, which promotes beta-cell function.

Conclusions:

  • Pancreatic pericyte Tcf7l2 activity is essential for maintaining beta-cell function and glucose homeostasis.
  • Pericytes secrete factors like BMP4 in a TCF7L2-dependent manner to support beta-cells.
  • Disruptions in the islet microenvironment, mediated by TCF7L2, may contribute to type 2 diabetes pathogenesis.