Inosine partially mimics the effects of glucose on ionic fluxes, electrical activity, and insulin release in mouse pancreatic B-cells

1987 ◽  
Vol 410 (4-5) ◽  
pp. 457-463 ◽  
Author(s):  
M. Bozem ◽  
M. -G. Garrino ◽  
J. -C. Henquin
Keyword(s):  
B Cells ◽  
Electrical Activity ◽  
Insulin Release ◽  
Ionic Fluxes ◽  
Pancreatic B Cells

Ontogeny of salivary peptide P-C like immunoreactivity in human pancreatic B-cells

1983 ◽  
Vol 103 (4) ◽  
pp. 552-557 ◽  
Author(s):  
Seiki Ito ◽  
Satoko Isemura ◽  
Eiichi Saitoh ◽  
Kazuo Sanada ◽  
Toshimitsu Suzuki ◽  
...  
Keyword(s):  
B Cells ◽  
Insulin Release ◽  
Protein C ◽  
Calcium Concentration ◽  
Salivary Protein ◽  
Human Pancreas ◽  
Amino Acid Residues ◽  
Salivary Peptide ◽  
Pancreatic B Cells ◽  
Foetal Pancreas

Abstract. An immunohistochemical study using antisera against proline rich salivary peptide P-C and insulin, glucagon, somatostatin and pancreatic polypeptide antisera was carried out on the foetal pancreas at different stages and on the newborn infant's, infant's, child's and adult pancreas to examine the time at which salivary peptide P-C like immunoreactivity appeared in the human pancreas. Salivary peptide P-C like immunoreactive cells first appeared as a few scattered cells in the foetal pancreas after 16 weeks of gestation and gradually increased in numbers during gestation. The cells corresponded only to insulin immunoreactive cells in the foetal, newborn infant's, infant's, child's and adult pancreas. Only some of the insulin immunoreactive cells in the foetal pancreas contained salivary peptide P-C like immunoreactivity while the majority of those in the infant's pancreas and all those in the child's and adult pancreas did so. The findings, together with the fact that the full sequence of salivary peptide P-C is identical to the COOH-terminal 44 amino acid residues of Salivary Protein C, led to the possibility that peptide P-C like immunoreactivity in the human pancreatic B-cells was not a moiety of the precursor of insulin and pro-insulin, but a moiety of Salivary Protein C. It has been suggested that, in saliva, Salivary Protein C aids in maintenance of the calcium concentration. Based on the hypothesis that peptide P-C like immunoreactivity in the human pancreatic B-cells may play some role in insulin release through the maintenance of the calcium concentration, the present finding seems to explain the fact that the mechanism for insulin release in the foetal pancreas is immature in spite of sufficient biosynthesis of insulin.

Role of CYP2E1 in ketone-stimulated insulin release in pancreatic B-cells

2004 ◽  
Vol 67 (5) ◽  
pp. 875-884 ◽  
Author(s):  
Diane J.Lees Murdock ◽  
Jacqueline Clarke ◽  
Peter R. Flatt ◽  
Yvonne A. Barnett ◽  
Christopher R. Barnett
Keyword(s):  
B Cells ◽  
Insulin Release ◽  
Pancreatic B Cells

scholarly journals Die ultrastrukturele, morfometriese evaluering van die mikrotubulere stelsel in gestimuleerde B-selle van die pankreas

1992 ◽  
Vol 11 (4) ◽  
pp. 127-135
Author(s):  
A. Crous ◽  
A. M. De Beer ◽  
E. J. Visser
Keyword(s):  
B Cells ◽  
Insulin Release ◽  
Insulin Response ◽  
High Magnification ◽  
Tissue Samples ◽  
Islet Tissue ◽  
Pancreatic B Cells ◽  
Complete Cell

The intracellular distribution of microtubules in pancreatic B-cells was studied morphometrically to elucidate the positive correlation between microtubular content and the rate of insulin release found by biochemical investigations. Rat islet tissue was glucose stimulated under in vivo and in vitro (isolated islets) conditions and tissue samples taken to represent both phases of the phasic insulin response. Electron micrographs (x40 000) of individual B-cells were assembled into montages to obtain complete cell profiles at high magnification.

Somatostatin inhibition of glucose-induced electrical activity in cultured rat islet cells

1977 ◽  
Vol 233 (5) ◽  
pp. C164-C171 ◽  
Author(s):  
Caroline S. Pace ◽  
Mary Murphy ◽  
Susan Conant ◽  
Paul E. Lacy
Keyword(s):  
Electrical Activity ◽  
Insulin Release ◽  
Spike Activity ◽  
Inhibitory Action ◽  
Islet Cells ◽  
Secretory Response ◽  
Adrenergic Blockade ◽  
Ionic Fluxes ◽  
Electrophysiological Studies ◽  
Stimulus Secretion Coupling

Electrophysiological studies of rat islet cells in monolayer culture were undertaken to determine the role of transmembranous ionic fluxes in the inhibitory action of somatostatin on insulin release. In the presence of somatotropin release inhibiting factor (SRIF) (2.5 nM), hyperpolarization occured with or without glucose (16.6 mM) in the medium. SRIF also inhibited the incidence of glucose-induced spike activity. The inhibitory action of SRIF occurred within 5 min and was readily reversible. An increase in extracellular K+ (5–13 mM) or Ca2+ (2.3–4.6 mM) prevented SRIF inhibition of glucose-induced electrical activity. The secretory response of cultured islets to glucose (16.6 mM) was completely inhibited by SRIF (2.5 nM). The presence of high [Ca2+]0 or [K+]0, enhanced insulin release in the presence of SRIF and glucose. Although phentolamine (5.0 μg/ml) did not block the inhibition of glucose-induced electrical responses by SRIF, it prevented the inhibitory action of epinephrine (0.2 μg/ml). It is concluded that the primary action of SRIF is to alter transmembranous cationic fluxes, as manifested by hyperpolarization and a decrease in the incidence of spike activity, which may prevent glucose from eliciting a normal secretory response. insulin secretion; epinephrine; alpha-adrenergic blockade; stimulus-secretion coupling Submitted on February 14, 1977

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