scholarly journals Oxidative stress induces p21 expression in pancreatic islet cells: possible implication in beta-cell dysfunction

Diabetologia ◽  
1999 ◽  
Vol 42 (9) ◽  
pp. 1093-1097 ◽  
Author(s):  
H. Kaneto ◽  
Y. Kajimoto ◽  
Y. Fujitani ◽  
T. Matsuoka ◽  
K. Sakamoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Beta Cell ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Beta Cell Dysfunction ◽  
Pancreatic Islet Cells ◽  
Cell Dysfunction

Beta Cell Dysfunction, Oxidative Stress and S6K1 Activation in Pancreas in the Zucker Obese Rat Model

2011 ◽  
pp. P2-480-P2-480
Author(s):  
Guido Lastra ◽  
Charles B Krueger ◽  
Camila Manrique ◽  
James R Sowers
Keyword(s):  
Oxidative Stress ◽  
Beta Cell ◽  
Rat Model ◽  
Beta Cell Dysfunction ◽  
Cell Dysfunction

scholarly journals Role for inducible cAMP early repressor in promoting pancreatic beta cell dysfunction evoked by oxidative stress in human and rat islets

Diabetologia ◽  
2011 ◽  
Vol 54 (9) ◽  
pp. 2337-2346 ◽  
Author(s):  
D. Favre ◽  
G. Niederhauser ◽  
D. Fahmi ◽  
V. Plaisance ◽  
S. Brajkovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Beta Cell Dysfunction ◽  
Rat Islets ◽  
Cell Dysfunction ◽  
Inducible Camp Early Repressor

Prostaglandin E2 regulates Foxo activity via the Akt pathway: implications for pancreatic islet beta cell dysfunction

Diabetologia ◽  
2006 ◽  
Vol 49 (12) ◽  
pp. 2959-2968 ◽  
Author(s):  
Z. X. Meng ◽  
J. X. Sun ◽  
J. J. Ling ◽  
J. H. Lv ◽  
D. Y. Zhu ◽  
...  
Keyword(s):  
Beta Cell ◽  
Prostaglandin E2 ◽  
Pancreatic Islet ◽  
Akt Pathway ◽  
Beta Cell Dysfunction ◽  
Islet Beta Cell ◽  
Cell Dysfunction ◽  
Pancreatic Islet Beta Cell

scholarly journals CXC chemokine ligand 12α-mediated increase in insulin secretion and survival of mouse pancreatic islets in response to oxidative stress through modulation of calcium uptake

2018 ◽  
Vol 70 (1) ◽  
pp. 191-204 ◽  
Author(s):  
Melita Vidakovic ◽  
Ernesto Caballero-Garrido ◽  
Mirjana Mihailovic ◽  
Jelena Arambasic-Jovanovic ◽  
Marija Sinadinovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Diabetes Diagnosis ◽  
Pancreatic Islet Cells ◽  
Pancreatic Cell ◽  
Cxcr4 Signaling

We examined whether CXCL12? improves insulin secretion by influencing the Ca2+ oscillation pattern and Ca2+ influx ([Ca2+]i), thereby enhancing the viability of pancreatic islet cells in oxidative stress. The islets of Langerhans were isolated from male OF1 mice and pretreated with 40 ng/mL of CXCL12? prior to exposure to 7.5 ?M hydrogen peroxide, which served to induce oxidative stress. Incubation of islets with CXCL12? induced pancreatic ?-cell proliferation and improved the ability of ?-cells to withstand oxidative stress. Consecutive treatments of isolated islets with hydrogen peroxide caused a decline in ?-cell functioning over time, while the CXCL12? pretreatment of islets exhibited a physiological response to high glucose that was comparable to control islets. The attenuated response of islets to a high D-glucose challenge was observed as a partial to complete abolishment of [Ca2+]i. Treatments with increasing concentrations of CXCL12? decreased the number of Ca2+ oscillations that lasted longer, thus pointing to an overall increase in [Ca2+]i, which was followed by increased insulin secretion. In addition, treatment of islets with CXCL12? enhanced the transcription rate for insulin and the CXCR4 gene, pointing to the importance of CXCL12/CXCR4 signaling in the regulation of Ca2+ intake and insulin secretion in pancreatic islet cells. We propose that a potential treatment with CXCL12? could help to remove preexisting glucotoxicity and associated temporary ?-cell stunning that might be present at the time of diabetes diagnosis in vivo.

scholarly journals Glucose-induced beta cell dysfunction in vivo in rats: link between oxidative stress and endoplasmic reticulum stress

Diabetologia ◽  
2012 ◽  
Vol 55 (5) ◽  
pp. 1366-1379 ◽  
Author(s):  
C. Tang ◽  
K. Koulajian ◽  
I. Schuiki ◽  
L. Zhang ◽  
T. Desai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Beta Cell ◽  
Beta Cell Dysfunction ◽  
Cell Dysfunction

Modulation of Specific Beta Cell Gene (Re)Expression during In Vitro Expansion of Human Pancreatic Islet Cells

2003 ◽  
Vol 12 (7) ◽  
pp. 799-807 ◽  
Author(s):  
Thomas Bouckenooghe ◽  
Brigitte Vandewalle ◽  
Bruno Lukowiak ◽  
Julie Kerr-Conte ◽  
Sandrine Beläich ◽  
...  
Keyword(s):  
Beta Cell ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Human Pancreatic Islet ◽  
In Vitro Expansion ◽  
Cell Gene

Abstract 483: Non-redundant and Opposing Roles of Group X and Group V Secretory Phospholipase A2s on Pancreatic Beta-cell Function

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Preetha Shridas ◽  
Victoria P Noffsinger ◽  
Nancy R Webb
Keyword(s):  
Beta Cell ◽  
Cell Lines ◽  
Pancreatic Islet ◽  
Cell Function ◽  
Islet Cells ◽  
Pancreatic Beta Cell ◽  
Pge2 Production ◽  
Pancreatic Islet Cells ◽  
Group V ◽  
Min6 Cells

Background: Group X and group V secretory phospholipase A2s (GX and GV sPLA2s) potently release arachidonic acid (AA) from the plasma membrane of intact cells. AA is an activator of glucose-stimulated insulin secretion (GSIS) by β-islet cells. However, the AA metabolite prostaglandin E2 (PGE2) is a known inhibitor of GSIS. Both GX and GV sPLA2s are expressed in mouse pancreatic islet cells. We previously demonstrated that GX sPLA2 negatively regulates GSIS by a PGE2-dependent mechanism. In this study we investigated whether GV sPLA2 similarly regulates GSIS. Methods and Results: GSIS was measured in pancreatic islet cells isolated from WT and GV sPLA2-deficient (GV KO) mice. To complement these studies, GSIS was also assessed in vitro using MIN6 pancreatic beta cell lines with or without GV sPLA2 overexpression or silencing. In marked contrast to our findings in GX KO mice, GSIS was significantly decreased in islets isolated from GV KO mice compared to WT mice. Similarly, there was a significant decrease in GSIS in MIN6 cells with siRNA-mediated GV sPLA2 suppression. Consistent with these findings, MIN6 cells overexpressing GV sPLA2 (MIN6-GV) showed a significant increase in GSIS compared to control cells. As expected, the amount of AA released into the media by MIN6-GV cells was significantly increased compared to control MIN6 cells. However, unlike MIN6 cells overexpressing GX sPLA2, MIN6-GV cells did not exhibit enhanced PGE2 production or decreased cAMP content compared to control MIN6 cells, despite similar amounts of sPLA2 activity produced by the two cell lines. Conclusions: We conclude that GX and GV sPLA2s play opposing and non-redundant roles in pancreatic β-cell function. Whereas GV sPLA2 activates GSIS, GX sPLA2 suppresses this process. This functional difference appears to be due to the extent to which AA generated by the respective sPLA2’s is coupled to PGE2 production.

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