title: Taurine regulates insulin release from pancreatic beta cell lines.
abstract: BACKGROUND
  Pancreatic beta-cells release insulin via an electrogenic response triggered by an increase in plasma glucose concentrations. The critical plasma glucose concentration has been determined to be approximately 3 mM, at which time both insulin and GABA are released from pancreatic beta-cells. Taurine, a beta-sulfonic acid, may be transported into cells to balance osmotic pressure. The taurine transporter (TauT) has been described in pancreatic tissue, but the function of taurine in insulin release has not been established. Uptake of taurine by pancreatic beta-cells may alter membrane potential and have an effect on ion currents. If taurine uptake does alter beta-cell current, it might have an effect on exocytosis of cytoplasmic vesicle. We wished to test the effect of taurine on regulating release of insulin from the pancreatic beta-cell.
  
  
  METHODS
  Pancreatic beta-cell lines Hit-TI5 (Syrian hamster) and Rin-m (rat insulinoma) were used in these studies. Cells were grown to an 80% confluence on uncoated cover glass in RPMI media containing 10% fetal horse serum. The cells were then adapted to a serum-free, glucose free environment for 24 hours. At that time, the cells were treated with either 1 mM glucose, 1 mM taurine, 1 mM glucose + 1 mM taurine, 3 mM glucose, or 3 mM glucose + 1 mM taurine. The cells were examined by confocal microscopy for cytoplasmic levels of insulin.
  
  
  RESULTS
  In both cell lines, 1 mM glucose had no effect on insulin levels and served as a control. Cells starved of glucose had a significant reduction (p<0.001) in the level of insulin, but this level was significantly higher than all other treatments. As expected, the 3 mM glucose treatment resulted in a statistically lower (p<0.001) insulin level than control cells. Interestingly, 1 mM taurine also resulted in a statistically lower level of insulin (p<0.001) compared to controls when either no glucose or 1 mM glucose was present. Cells treated with 1 mM taurine plus 3 mM glucose showed a level of insulin similar to that of 3 mM glucose alone.
  
  
  CONCLUSIONS
  Taurine administration can alter the electrogenic response in beta-cell lines, leading to a change in calcium homeostasis and a subsequent decrease in intracellular insulin levels. The consequence of these actions could represent a method of increasing plasma insulin levels leading to a decrease in plasma glucose levels.
authors.affiliation: Department of Biology, College of Staten Island, The City University of New York, 2800 Victory Boulevard, Staten Island, NY 10314, USA. William.Lamoreaux@csi.cuny.edu
authors.forename: William J
authors.initials: WJ
authors.lastname: L'Amoreaux
authors.forename: Christina
authors.initials: C
authors.lastname: Cuttitta
authors.forename: Allison
authors.initials: A
authors.lastname: Santora
authors.forename: Jonathan F
authors.initials: JF
authors.lastname: Blaize
authors.forename: Janto
authors.initials: J
authors.lastname: Tachjadi
authors.forename: Abdeslem
authors.initials: A
authors.lastname: El Idrissi
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002460:Cell Line; D006224:Cricetinae; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism; D026901:Membrane Transport Proteins / Q000378:metabolism; D051381:Rats; D013654:Taurine / Q000378:metabolism / Q000494:pharmacology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism; D000099247:Taurine Transporters
chemical_list: D001786:Blood Glucose; D005947:Glucose; D007328:Insulin; D008562:Membrane Glycoproteins; D026901:Membrane Transport Proteins; D013654:Taurine; D005680:gamma-Aminobutyric Acid; D000099247:Taurine Transporters
references.citation: Adv Exp Med Biol. 2009;643:207-15
references.pmid: 19239151
references.citation: Curr Opin Investig Drugs. 2003 Oct;4(10):1166-72
references.pmid: 14649207
references.citation: Annu Rev Biochem. 1995;64:689-719
references.pmid: 7574498
references.citation: Brain Res. 2000 May 12;864(2):298-307
references.pmid: 10802037
references.citation: PLoS One. 2008;3(10):e3543
references.pmid: 18958155
references.citation: Neuroscience. 2008 Oct 15;156(3):693-9
references.pmid: 18727952
references.citation: Neurochem Res. 2004 Jan;29(1):27-63
references.pmid: 14992263
references.citation: Br J Pharmacol. 2000 Jun;130(4):827-34
references.pmid: 10864889
references.citation: Amino Acids. 2008 Feb;34(2):321-8
references.pmid: 16955229
references.citation: Adv Exp Med Biol. 2009;643:353-8
references.pmid: 19239166
references.citation: Endocrinology. 1991 Nov;129(5):2521-9
references.pmid: 1682137
references.citation: Diabetes. 2009 Dec;58(12):2813-9
references.pmid: 19720793
references.citation: Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):5744-8
references.pmid: 1631055
references.citation: Diabetes. 2004 Jul;53(7):1743-53
references.pmid: 15220198
references.citation: Diabetologia. 2004 Oct;47(10):1831-7
references.pmid: 15502919
references.citation: Neuroscience. 2003;120(3):635-42
references.pmid: 12895504
references.citation: Adv Exp Med Biol. 2006;583:315-22
references.pmid: 17153616
references.citation: Neurochem Res. 2004 Jan;29(1):189-97
references.pmid: 14992278
references.citation: Cell Mol Life Sci. 2002 Nov;59(11):1803-18
references.pmid: 12530515
references.citation: J Gen Physiol. 2007 Mar;129(3):221-31
references.pmid: 17296927
references.citation: J Physiol. 2007 Dec 1;585(Pt 2):539-48
references.pmid: 17962336
references.citation: Surgery. 2004 Sep;136(3):585-92
references.pmid: 15349106
references.citation: Adv Exp Med Biol. 2003;526:515-25
references.pmid: 12908638
references.citation: Neurosci Lett. 2008 May 2;436(1):19-22
references.pmid: 18375059