scholarly journals Bimodal role of conventional protein kinase C in insulin secretion from rat pancreatic β cells

2004 ◽  
Vol 561 (1) ◽  
pp. 133-147 ◽  
Author(s):  
Hui Zhang ◽  
Masahiro Nagasawa ◽  
Satoko Yamada ◽  
Hideo Mogami ◽  
Yuko Suzuki ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Insulin Secretion ◽  
Protein Kinase ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Kinase C

Role of protein kinase C in the regulation of insulin secretion

1989 ◽  
Vol 17 (1) ◽  
pp. 61-63 ◽  
Author(s):  
PETER M. JONES ◽  
SIMON L. HOWELL
Keyword(s):  
Protein Kinase C ◽  
Insulin Secretion ◽  
Protein Kinase ◽  
Kinase C

scholarly journals A re-assessment of the role of protein kinase C in glucose-stimulated insulin secretion

1987 ◽  
Vol 246 (2) ◽  
pp. 489-493 ◽  
Author(s):  
C S T Hii ◽  
P M Jones ◽  
S J Persaud ◽  
S L Howell
Keyword(s):  
Protein Kinase C ◽  
Insulin Secretion ◽  
Protein Kinase ◽  
Phorbol Esters ◽  
Pancreatic Beta Cell ◽  
Cell Types ◽  
Protein Kinase Activity ◽  
Kinase C ◽  
Rat Islets Of Langerhans

Isolated rat islets of Langerhans which had been pretreated with 200 nM-phorbol 12-myristate 13-acetate (PMA) for 20-24 h, a treatment reported in other cell types to deplete cells of protein kinase C activity, were found not to contain detectable Ca2+/phospholipid-dependent protein kinase activity. These islets did not secrete insulin in response to a subsequent exposure to PMA (0.1 or 1 microM) during a 30 min incubation, although insulin secretion could be stimulated by 20 mM-glucose, a response which was enhanced by 20 microM-forskolin. PMA-pretreated islets that had been permeabilized by high-voltage discharge showed unimpaired secretory responses to an increase in Ca2+ concentration, cyclic AMP and forskolin. These results suggest that (i) pretreatment of islets with tumour-promoting phorbol esters may be a useful means of investigating the role of protein kinase C in stimulus-secretion coupling in the pancreatic beta-cell and (ii) protein kinase C may not play an essential role in glucose-induced insulin secretion.

Protein kinase C-dependent and -independent inhibition of Ca2+ influx by phorbol ester in rat pancreatic β-cells

2001 ◽  
Vol 13 (3) ◽  
pp. 199-205 ◽  
Author(s):  
Junko Nakamura ◽  
Toshihiro Suda ◽  
Yoshiji Ogawa ◽  
Teruko Takeo ◽  
Sechiko Suga ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Phorbol Ester ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Kinase C

scholarly journals Vasopressin potentiates corticotropin-releasing hormone-induced insulin release from mouse pancreatic β-cells

2008 ◽  
Vol 197 (2) ◽  
pp. 231-239 ◽  
Author(s):  
Anne-Marie O'Carroll ◽  
Gillian M Howell ◽  
Emma M Roberts ◽  
Stephen J Lolait
Keyword(s):  
Insulin Secretion ◽  
Protein Kinase ◽  
Corticotropin Releasing Hormone ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Releasing Hormone ◽  
Kinase C ◽  
Mouse Pancreatic Islets ◽  
M3 Receptor ◽  
Pituitary Adrenal Axis

Arginine vasopressin (AVP) and corticotropin-releasing hormone (CRH) have both been implicated in modulating insulin secretion from pancreatic β-cells. In the present study, we investigated the insulin-secreting activities of AVP and CRH in wild-type and AVP VIb receptor knockout mice. Both neuropeptides stimulated insulin secretion from isolated mouse pancreatic islets. The response of islets to CRH was increased fourfold by concomitant incubation with a subthreshold dose of AVP that alone did not stimulate insulin secretion. Activation of the endogenously expressed M3 receptor by the cholinergic agonist carbachol also potentiated CRH-induced insulin secretion, indicating that the phenomenon may be pathway specific (i.e. Ca2+-phospholipase C) rather than agonist specific. The protein kinase C (PKC) inhibitors Ro-31-8425 and bisindolylmaleimide I attenuated the potentiating effect of AVP on CRH-stimulated insulin secretion and blocked AVP-stimulated insulin secretion. A possible interaction between the PKC and protein kinase A pathways was also investigated. The phorbol ester phorbol myristate acetate (PMA) stimulated insulin secretion, while the addition of both PMA and CRH enhanced insulin secretion over that measured with either PMA or CRH alone. Additionally, no AVP potentiation of CRH-stimulated insulin secretion was observed upon incubation in Ca2+-free Krebs–Ringer buffer. Taken together, the present study suggests a possible synergism between AVP and CRH to release insulin from pancreatic β-cells that relies at least in part on activation of the PKC signaling pathway and is dependent on extracellular Ca2+. This is the first example of a possible interplay between the AVP and CRH systems outside of the hypothalamic–pituitary–adrenal axis.

scholarly journals Translocation Inhibitors Define Specificity of Protein Kinase C Isoenzymes in Pancreatic β-Cells

1997 ◽  
Vol 272 (3) ◽  
pp. 1417-1420 ◽  
Author(s):  
Michael Yedovitzky ◽  
Daria Mochly-Rosen ◽  
John A. Johnson ◽  
Mary O. Gray ◽  
Dorit Ron ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Kinase C

scholarly journals Protein kinase C-θ knockout decreases serum IL-10 levels and inhibits insulin secretion from islet β cells

Islets ◽  
2021 ◽  
Vol 13 (1-2) ◽  
pp. 24-31
Author(s):  
Feng Hong ◽  
Yang Yang ◽  
Baiyi Chen ◽  
Peng Li ◽  
Guoguang Wang ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Insulin Secretion ◽  
Protein Kinase ◽  
Β Cells ◽  
Kinase C

Role of Protein Kinase C Isoenzymes in Fatty Acid Stimulation of Insulin Secretion

Pancreas ◽  
2000 ◽  
Vol 20 (3) ◽  
pp. 256-263 ◽  
Author(s):  
Eva D Littman ◽  
Suresh Pitchumoni ◽  
Marc R Garfinkel ◽  
Emmanuel C Opara
Keyword(s):  
Protein Kinase C ◽  
Insulin Secretion ◽  
Fatty Acid ◽  
Protein Kinase ◽  
Kinase C ◽  
Stimulation Of

scholarly journals Involvement of Protein Kinase C β2 in c-mycInduction by High Glucose in Pancreatic β-Cells

2001 ◽  
Vol 277 (5) ◽  
pp. 3680-3685 ◽  
Author(s):  
Hideaki Kaneto ◽  
Kiyoshi Suzuma ◽  
Arun Sharma ◽  
Susan Bonner-Weir ◽  
George L. King ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
High Glucose ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Kinase C
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