3-(Alkylamino)-4H-pyrido[4,3-e]1,2,4-thiadiazine 1,1-dioxides as powerful inhibitors of insulin release from rat pancreatic B-cells: a new class of potassium channel openers?

1993 ◽  
Vol 36 (21) ◽  
pp. 3211-3213 ◽  
Author(s):  
Bernard Pirotte ◽  
Pascal de Tullio ◽  
Philippe Lebrun ◽  
Marie Helene Antoine ◽  
Jeanine Fontaine ◽  
...  
1983 ◽  
Vol 103 (4) ◽  
pp. 552-557 ◽  
Author(s):  
Seiki Ito ◽  
Satoko Isemura ◽  
Eiichi Saitoh ◽  
Kazuo Sanada ◽  
Toshimitsu Suzuki ◽  
...  

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.


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

1992 ◽  
Vol 11 (4) ◽  
pp. 127-135
Author(s):  
A. Crous ◽  
A. M. De Beer ◽  
E. J. Visser

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.


1988 ◽  
Vol 156 (2) ◽  
pp. 283-286 ◽  
Author(s):  
Philippe Lebrun ◽  
Vincent Devreux ◽  
Marcel Hermann ◽  
André Herchuelz

1989 ◽  
Vol 121 (3) ◽  
pp. 479-485 ◽  
Author(s):  
D. G. Lambert ◽  
T. W. Atkins

ABSTRACT The effects of the islet cell hormones glucagon, somatostatin-28 and pancreatic polypeptide on insulin secretion from cultured cloned pancreatic B cells (HIT-T15 and RINm5F) have been investigated. Glucagon stimulates the secretion of insulin from HIT-T15 cells in the absence and presence of glucose and from RINm5F cells in the absence and presence of glyceraldehyde. HIT-T15 cells were more sensitive to the stimulatory effect of glucagon than RINm5F cells. Somatostatin-28 and pancreatic polypeptide, both alone and in combination, reduced glucose- and glucagon-stimulated insulin release from HIT-T15 cells and glyceraldehyde- and glucagon-stimulated insulin release from RINm5F cells. HIT-T15 cells were more sensitive to the inhibitory actions of somatostatin-28 and pancreatic polypeptide than RINm5F cells. This study supports the hypothesis that insulin release from normal B cells may be modified by the paracrine activity of islet hormones, glucagon, somatostatin and pancreatic polypeptide and probably occurs before any fine tuning imposed by subsequently released insulin. Journal of Endocrinology (1989) 121, 479–485


2019 ◽  
Vol 178 ◽  
pp. 223-224
Author(s):  
Philippe Trechot ◽  
Jean-Baptiste Conart ◽  
Fanny Trechot

1998 ◽  
Vol 1370 (1) ◽  
pp. 8-16 ◽  
Author(s):  
Gisela Drews ◽  
Günther Zempel ◽  
Peter Krippeit-Drews ◽  
Stefan Britsch ◽  
Gillian L Busch ◽  
...  

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