This photograph shows a mouse pancreatic islet, an often spherical group of hormone-producing cells. Insulin is labelled here in green, glucagon in red, and the nuclei in blue.
The diagram shows the structural differences between rat islets (top) and humans islets (bottom) as well as the ventral part (left) and the dorsal part (right) of the pancreas. Different cell types are colour coded. Rodent islets, unlike the human ones, show the characteristic insulin core.
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, hemalum-eosin stain.
Illustration of dog pancreas. 250x.
The endocrine (i.e., hormone-producing) cells of the pancreas are grouped in the islets of Langerhans. Discovered in 1869 by the famous 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; their combined weight is 1 to 1.5 grams.
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).
Paracrine feedback
The paracrine feedback system of the islets of Langerhans has the following structure:[2]
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
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 behavior of dispersed cells[3].
As a treatment for type I diabetes
Because the beta cells in the 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[4]. Rachel Harris, islet cell recipient, was transplanted at the Diabetes Research Institute in Miami, Florida. In June of 2004, Rachel became the world's longest surviving insulin-free diabetic according to the Miami Herald (published Feb. 13, 2004).[5]
Islet transplantation currently requires potent immunosuppression to prevent host rejection of donor islets. An alternative source of beta cells, such an islets derived from adult stem cells or progenitor cells of a diabetic would eliminate the need for immuosuppressive therapy, and be safer for diabetics.[6].
Transplantation
With the possibility of restoring beta cells, the Chicago Project headed at University of Illinois at Chicago Medical Center is investigating ways to regenerate beta cells in vivo. With that being said, beta cells experience apoptosis early and thus are destroyed within a normal-functioning pancreas. The source of this seems to come from the transfer of Pander, a gene that works by attaching to RNA[7]. Pander, when active, causes the beta cells to be blocked at S phase, which induces apoptosis. This loss of beta cell mass eventually leads to a loss of most of the transplanted beta cells.
^ Elayat AA, el-Naggar MM, Tahir M (1995). "An immunocytochemical and morphometric study of the rat pancreatic islets". J. Anat.186 ( Pt 3): 629–37. PMID 7559135.
^ Wang, Michael B.; Bullock, John; Boyle, Joseph R. (2001). Physiology. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-683-30603-0.
^ Pérez-Armendariz M, Roy C, Spray DC, Bennett MV (1991). "Biophysical properties of gap junctions between freshly dispersed pairs of mouse pancreatic beta cells". Biophys. J.59 (1): 76–92. PMID 2015391.
^ Meloche RM (2007). "Transplantation for the treatment of type 1 diabetes". World J. Gastroenterol.13 (47): 6347–55. doi:10.3748/wjg.13.6347. PMID 18081223.
^ Chatenoud L (2008). "Chemical immunosuppression in islet transplantation--friend or foe?". N. Engl. J. Med.358 (11): 1192–3. doi:10.1056/NEJMcibr0708067. PMID 18337609.
^ Cao X, Gao Z, Robert CE, et al (2003). "Pancreatic-derived factor (FAM3B), a novel islet cytokine, induces apoptosis of insulin-secreting beta-cells". Diabetes52 (9): 2296–303. doi:10.2337/diabetes.52.9.2296. PMID 12941769.