Beta cell

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Beta cell
Mouse islet LM SolimenaLab.jpg
The photo above shows a mouse pancreatic islet as seen by light microscopy. Beta cells can be recognised by the green insulin staining. Glucagon is labelled in red and the nuclei in blue.
Islet.png
An islet of Langerhans in a pig. 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.
Details
Latinendocrinocytus B; insulinocytus
Identifiers
CodeTH H3.04.02.0.00026
Anatomical terminology
 
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Beta cell
Mouse islet LM SolimenaLab.jpg
The photo above shows a mouse pancreatic islet as seen by light microscopy. Beta cells can be recognised by the green insulin staining. Glucagon is labelled in red and the nuclei in blue.
Islet.png
An islet of Langerhans in a pig. 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.
Details
Latinendocrinocytus B; insulinocytus
Identifiers
CodeTH H3.04.02.0.00026
Anatomical terminology

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

Function[edit]

The primary function of a beta cell is to store and release insulin. Insulin is a hormone that brings about effects which reduce blood glucose concentration. Beta cells can respond quickly to spikes in blood glucose concentrations by secreting some of their stored insulin while simultaneously producing more.

Control of Insulin Secretion[edit]

Voltage gated calcium ion channels and ATP-sensitive potassium ion channels are embedded in the cell surface membrane of beta cells. These ATP-sensitive potassium ion channels are normally open and the calcium ion channels are normally closed. Potassium ions diffuse out of the cell, down their concentration gradient, making the inside of the cell more negative with respect to the outside (as potassium ions carry a positive charge). At rest, this creates a potential difference across the cell surface membrane of -70mV.

When the glucose concentration outside the cell is high, glucose molecules move into the cell by facilitated diffusion, down its concentration gradient through the GLUT2 transporter. Since beta cells use glucokinase to catalyze the first step of glycolysis, metabolism only occurs around physiological blood glucose levels and above. Metabolism of the glucose produces ATP, which increases the ATP to ADP ratio.

The ATP-sensitive potassium ion channels close when this ratio rises. This means that potassium ions can no longer diffuse out of the cell.[1] As a result, the potential difference across the membrane becomes more positive (as potassium ions accumulate inside the cell). This change in potential difference opens the voltage-gated calcium channels, which allows calcium ions from outside the cell to diffuse in down their concentration gradient. When the calcium ions enter the cell, they cause vesicles containing insulin to move to, and fuse with, the cell surface membrane, releasing insulin by exocytosis.[2]

Other Hormones Secreted by Beta Cells[edit]

Pathology[edit]

Diabetes mellitus can be experimentally induced for research purposes by streptozotocin or alloxan, which are specifically toxic to beta cells.

See also[edit]

References[edit]

  1. ^ Keizer J, Magnus G (1989). "ATP-sensitive potassium channel and bursting in the pancreatic beta cell. A theoretical study.". Biophysical Journal 56 (2): 229–242. doi:10.1016/S0006-3495(89)82669-4. PMC 1280472. PMID 2673420. 
  2. ^ Lang V, Light PE (2010). "The molecular mechanisms and pharmacotherapy of ATP-sensitive potassium channel gene mutations underlying neonatal diabetes.". Pharmgenomics. Pers. Med. 3: 145–61. doi:10.2147/PGPM.S6969. PMID 23226049. 
  3. ^ Ido Y, Vindigni A, Chang K, Stramm L, Chance R, Heath WF et al. (1997). "Prevention of vascular and neural dysfunction in diabetic rats by C-peptide". Science 277 (5325): 563–6. doi:10.1126/science.277.5325.563. PMID 9228006. 
  4. ^ 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. doi:10.1210/jcem-56-1-60. PMID 6336620. 
  5. ^ 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. 
  6. ^ "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 Journal. Retrieved 2014-04-21. 
  7. ^ 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. 

External links[edit]