Islets of Langerhans

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A porcine islet of Langerhans.  The left image is a brightfield image created using hematoxylin stain; nuclei are dark circles and the acinar pancreatic tissue is darker than the islet tissue.  The right image is the same section stained by immunofluorescence against insulin, indicating beta cells.
A porcine islet of Langerhans. The left image is a brightfield image created using hematoxylin stain; nuclei are dark circles and the acinar pancreatic tissue is darker than the islet tissue. The right image is the same section stained by immunofluorescence against insulin, indicating beta cells.
Islets of Langerhans, haemalum-eosin stain.
Islets of Langerhans, haemalum-eosin stain.
Section of pancreas of dog. X 250.
Section of pancreas of dog. X 250.

The endocrine (i.e., hormone-producing) cells of the pancreas are grouped in the islets of Langerhans. Discovered in 1869 by the German pathological anatomist Paul Langerhans, the islets of Langerhans constitute approximately 1 to 2% of the mass of the pancreas. There are about one million islets in a healthy adult human pancreas, which are distributed evenly throughout the organ, and their combined weight is 1 to 1.5 grams.

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Hormones produced in the Islets of Langerhans are secreted directly into the blood flow by (at least) four different types of cells:

Islets can influence each other through paracrine and autocrine communication, and beta-cells are coupled electrically to beta-cells (but not to other cell-types).

The paracrine feedback system of the islets of Langerhans has the following structure:

  • Insulin: Activates beta cells and inhibits alpha cells.
  • Glucagon: Activates alpha which activates beta cells and delta cells.
  • Somatostatin: Inhibits alpha cells and beta cells.

Electrical activity of pancreatic islets has been studied using patch clamp techniques, and it has turned out that the behavior of cells in intact islets differs significantly from the behaviour of dispersed cells.

Since the beta cells in islets of Langerhans are destroyed in type I diabetes, clinicians and researchers are actively pursuing islet transplantation technology as a means of curing this disease.

Islet transplantation which currently requires immune suppression would be safer for type-1 diabetics if the need for lifelong immune suppression were eliminated.

With the possiblity of restoring beta cells, the Chicago Project headed at University of Illinois at Chicago Medical Center is probing for a way to regenerate beta cells in the islets and have them cultivate on their own within a human pancreas. With that being said, beta cells experience apoptosis early and thus become destroyed within a normal-functioning pancreas. The source of this seems to come from the transfer of Pander, a gene that enters in by attaching to RNA. This process of RNA transportation can be found in the glucose that bombards the beta cells. The genetic encoding found within Pander causes the beta cells to stop during the S phase of mitosis and head straight to apotasis. This ceases much of the reproduction of beta cells within the Islets.

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