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Contents
1 Function
o 1.1 Control of insulin secretion
o 1.2 Other hormones secreted by beta cells
2 Pathology
3 See also
4 References
5 External links
Function
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.
Voltage-gated calcium 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.[1]
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.[2] 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.[3]
Pathology
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.[7][8]
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.
See also
Insulin
Amylin
C-peptide
Gastric inhibitory polypeptide receptor
ATP-sensitive potassium channel
List of terms associated with diabetes
Guangxitoxin
Alpha cell
References
1. 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): 24892495. doi:10.1172/JCI118308.
2. Keizer J, Magnus G (1989). "ATP-sensitive potassium channel and bursting in the
pancreatic beta cell. A theoretical study.". Biophysical Journal 56 (2): 229242.
doi:10.1016/S0006-3495(89)82669-4. PMC 1280472. PMID 2673420.
3. Lang V, Light PE (2010). "The molecular mechanisms and pharmacotherapy of ATP-
sensitive potassium channel gene mutations underlying neonatal diabetes.".
Pharmgenomics. Pers. Med. 3: 14561. doi:10.2147/PGPM.S6969. PMID 23226049.
4. 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): 5636. doi:10.1126/science.277.5325.563. PMID 9228006.
5. 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): 607. doi:10.1210/jcem-56-1-60.
PMID 6336620.
6. 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): 19. doi:10.1016/0006-
291X(91)91325-7. PMID 1679326.
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.
8. 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): 90817. doi:10.1016/0026-0495(91)90065-5.
PMID 1895955.
External links
Pancreatic beta cells at the US National Library of Medicine Medical Subject
Headings (MeSH)
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t
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Thyroid isthmus
Thyroid Follicular cell
gland Parafollicular cell
Chief cell
Parathyroid
Oxyphil cell
gland
Zona glomerulosa
Zona fasciculata
Cortex
Adrenal Zona reticularis
gland
Chromaffin cell
Medulla
Testicle
o Leydig cell
o Sertoli cell
Ovary
Gonads
o Theca interna
o Granulosa cell
o Corpus luteum
Alpha cell
Beta cell
Islets of PP cell
pancreas Delta cell
Epsilon cell
Pinealocyte
Pineal
Corpora arenacea
gland
Enteroendocrine cell
Paraganglia
Other o Organ of Zuckerkandl
Placenta
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Index of hormones
Glands
Hormones
o thyroid
intermediates
Description metabolism
o mineralocorticoids
Physiology
Development
Diabetes
Congenital
Neoplasms and cancer
Disease
Other
Symptoms and signs
Procedures
Drugs
o calcium balance
o corticosteroids
Treatment
o oral hypoglycemics
o pituitary and hypothalamic
o thyroid
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