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.
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
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. 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.
Other Hormones Secreted by Beta Cells
- C-peptide, which is secreted into the bloodstream in equimolar quantities to insulin. C-peptide helps to prevent neuropathy and other vascular deterioration related symptoms of diabetes mellitus. A practitioner would measure the levels of C-peptide to obtain an estimate for the viable beta cell mass.
- Amylin, also known as islet amyloid polypeptide (IAPP). The function of amylin is to slow the rate of glucose entering the bloodstream. Amylin can be described as a synergistic partner to insulin, where insulin regulates long term food intake and amylin regulates short term food intake.
- Type 1 diabetes mellitus, also known as insulin dependent diabetes, is believed to be caused by an autoimmune response where the body's own immune system attacks the beta cells and destroys them. This means the body can no longer produce and secrete insulin into the blood and regulate the blood glucose concentration.
- Type 2 diabetes mellitus, also known as non insulin dependent diabetes, is caused by many factors including: age; family history; obesity and consuming a diet high in simple sugars. The beta cells, however, can still secrete insulin but the body has developed a resistance and its response to insulin has declined. It is believed to be due to the decline of specific receptors on the surface of the liver and muscle cells which lose their ability to respond to insulin that circulates in the blood.
- Insulinoma is a rare tumor derived the neoplasia of beta cells. Insulinomas are usually benign, but may be medically significant and even life-threatening due to recurrent and prolonged attacks of hypoglycemia.
Diabetes mellitus can be experimentally induced for research purposes by streptozotocin or alloxan, which are specifically toxic to beta cells.
- ↑ De Vos, Anick; Heimberg, Harry; Quartier, Erik; Huypens, Peter; Bouwens, Luc; Pipeleers, Daniel; Schuit, Frans (1995). "Human and rat beta cells differ in glucose transporter but not in glucokinase gene expression". Journal of Clinical Investigation 96 (November): 2489–2495. doi:10.1172/JCI118308.
- ↑ 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. PMC 1280472. PMID 2673420. doi:10.1016/S0006-3495(89)82669-4.
- ↑ 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. PMID 23226049. doi:10.2147/PGPM.S6969.
- ↑ 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. PMID 9228006. doi:10.1126/science.277.5325.563.
- ↑ 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. doi:10.1210/jcem-56-1-60.
- ↑ 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. PMID 1679326. doi:10.1016/0006-291X(91)91325-7.
- ↑ "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.
- ↑ 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. PMID 1895955. doi:10.1016/0026-0495(91)90065-5.