Beta cells

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The photography shows a beta cell as seen by electron microscopy. The nucleus is located at the bottom left and insulin granules (dark spheres) are mostly towards the top right.
The photo above shows a mouse pancreatic islet as seen by light microscopy. β cells can be recognised by the green insulin staining. Glucagon is labelled in red and the nuclei in blue.
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.

Beta cells (beta-cells, β-cells) are a type of cell in the pancreas in areas called the islets of Langerhans. They make up 65-80% of the cells in the islets.

Contents

[edit] Function

Beta cells make and release insulin, a hormone that controls the level of glucose in the blood. There is a baseline level of insulin maintained by the pancreas, but it can respond quickly to spikes in blood glucose by releasing stored insulin while simultaneously producing more. The response time is fairly quick, taking approximately 10 minutes.

Apart from insulin, beta cells release C-peptide, a byproduct of insulin production, into the bloodstream in equimolar quantities. C-peptide helps to prevent neuropathy, and other symptoms of diabetes related to vascular deterioration[1]. Measuring the levels of C-peptide can give a practitioner an idea of the viable beta cell mass.[2]

β-cells also produce amylin,[3] also known as IAPP, islet amyloid polypeptide. Amylin functions as part of the endocrine pancreas and contributes to glycemic control. Amylin's metabolic function is now somewhat well characterized as an inhibitor of the appearance of nutrient [especially glucose] in the plasma. It thus functions as a synergistic partner to insulin. Whereas insulin regulates long term food intake, increased amylin decreases food intake in the short term.

[edit] Pathology

  • Diabetes mellitus type 1 is caused by the destruction or dysfunction of insulin-producing beta cells by the cells of the immune system.

[edit] Research

Much research is being done in the field of beta-cell physiology and pathology. One major research topic is its effects on diabetes. Many researchers are trying to find ways to use these beta-cells to help control or prevent diabetes. A major topic is the replication of adult beta-cells and the application of these to diabetes. The Larry L. Hillblom Islet Research Center at UCLA[6] is a leading research center in the field, within the Diabetes and Endocrinology Research Center[7], directed by Dr. Peter Butler. [8]

A team science effort also exists, known as the Beta Cell Biology Consortium (BCBC).[9] The BCBC is responsible for facilitating interdisciplinary approaches that will advance the understanding of pancreatic islet development and function. The long-term goal of the BCBC is to develop a cell-based therapy for insulin delivery.

In a study presented on June 8, 2008 at the American Diabetes Association’s 68th Scientific Sessions, a team showed that mice lacking insulin receptors in their beta cells had problems in the processing of insulin leading to excess, unprocessed levels of the hormone. Unprocessed insulin is unable to properly control glucose levels in the body. High circulating levels of unprocessed insulin and insulin resistance, a condition in which normal amounts of insulin are inadequate to produce a normal insulin response, are both known to be early indicators of type 2 diabetes.[10]

[edit] See also

[edit] References

  1. ^ Y. Ido, A. Vindigni, K. Chang, L. Stramm, R. Chance, W. F. Heath, R. D. DiMarchi, E. Di Cera, J. R. Williamson. 1997. Prevention of Vascular and Neural Dysfunction in Diabetic Rats by C-Peptide. Science, Vol. 277. no. 5325, pp. 563 - 566.
  2. ^ Hoogwerf B, Goetz F (1983). "Urinary C-peptide: a simple measure of integrated insulin production with emphasis on the effects of body size, diet, and corticosteroids". J Clin Endocrinol Metab 56 (1): 60–7. PMID 6336620. 
  3. ^ Moore C, Cooper G (1991). "Co-secretion of amylin and insulin from cultured islet beta-cells: modulation by nutrient secretagogues, islet hormones and hypoglycemic agents". Biochem Biophys Res Commun 179 (1): 1–9. doi:10.1016/0006-291X(91)91325-7. PMID 1679326. 
  4. ^ "U.K. prospective diabetes study 16. Overview of 6 years' therapy of type II diabetes: a progressive disease. U.K. Prospective Diabetes Study Group". Diabetes 44 (11): 1249–58. 1995. doi:10.2337/diabetes.44.11.1249. PMID 7589820. 
  5. ^ Rudenski A, Matthews D, Levy J, Turner R (1991). "Understanding "insulin resistance": both glucose resistance and insulin resistance are required to model human diabetes". Metabolism 40 (9): 908–17. doi:10.1016/0026-0495(91)90065-5. PMID 1895955. 
  6. ^ The Larry L. Hillblom Islet Research Center
  7. ^ The DERC Homepage has moved
  8. ^ Faculty
  9. ^ Beta Cell Biology Consortium
  10. ^ Newswise: Beta Cell Defect Linked to Type 2 Diabetes Retrieved on June 8, 2008.

[edit] External links

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