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 In Vivo ZIMIR Imaging of Mouse Pancreatic Islet Cells Shows Oscillatory Insulin Secretion

2021 ◽  
Vol 12 ◽  
Author(s):  
Shiuhwei Chen ◽  
ZhiJiang Huang ◽  
Harrison Kidd ◽  
Min Kim ◽  
Eul Hyun Suh ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Cell Mass ◽  
Beta Cell Mass ◽  
Pancreatic Islet Cells ◽  
Systemic Delivery ◽  
Β Cells ◽  
Spatiotemporal Resolution

Appropriate insulin secretion is essential for maintaining euglycemia, and impairment or loss of insulin release represents a causal event leading to diabetes. There have been extensive efforts of studying insulin secretion and its regulation using a variety of biological preparations, yet it remains challenging to monitor the dynamics of insulin secretion at the cellular level in the intact pancreas of living animals, where islet cells are supplied with physiological blood circulation and oxygenation, nerve innervation, and tissue support of surrounding exocrine cells. Herein we presented our pilot efforts of ZIMIR imaging in pancreatic islet cells in a living mouse. The imaging tracked insulin/Zn2+ release of individual islet β-cells in the intact pancreas with high spatiotemporal resolution, revealing a rhythmic secretion activity that appeared to be synchronized among islet β-cells. To facilitate probe delivery to islet cells, we also developed a chemogenetic approach by expressing the HaloTag protein on the cell surface. Finally, we demonstrated the application of a fluorescent granule zinc indicator, ZIGIR, as a selective and efficient islet cell marker in living animals through systemic delivery. We expect future optimization and integration of these approaches would enable longitudinal tracking of beta cell mass and function in vivo by optical imaging.

Dietary fatty acids modify insulin secretion of rat pancreatic islet cells in vitro

2002 ◽  
Vol 25 (5) ◽  
pp. 436-441 ◽  
Author(s):  
F. J. Tinahones ◽  
A. Pareja ◽  
F. J. Soriguer ◽  
J. M. Gómez-Zumaquero ◽  
F. Cardona ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Dietary Fatty Acids ◽  
Pancreatic Islet Cells ◽  
Rat Pancreatic Islet

scholarly journals Enterovirus infection in human pancreatic islet cells, islet tropism in vivo and receptor involvement in cultured islet beta cells

Diabetologia ◽  
2004 ◽  
Vol 47 (2) ◽  
pp. 225-239 ◽  
Author(s):  
P. Ylipaasto ◽  
K. Klingel ◽  
A. M. Lindberg ◽  
T. Otonkoski ◽  
R. Kandolf ◽  
...  
Keyword(s):  
Beta Cells ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Enterovirus Infection ◽  
Islet Beta Cells ◽  
Human Pancreatic Islet

scholarly journals Pancreatic islet cell autophagy during aging in rats

2013 ◽  
Vol 36 (2) ◽  
pp. 72 ◽  
Author(s):  
Shuang Wang ◽  
Qian-qian Sun ◽  
Bing Xiang ◽  
Xiu-Jun Li
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Pancreatic Islet ◽  
Islet Cell ◽  
Islet Cells ◽  
Cell Structure ◽  
Fasting Blood Glucose ◽  
Pancreatic Islet Cell ◽  
Pancreatic Cell ◽  
Old Rats

Purpose: Autophagy induces pancreatic β cell death. The purpose of the present study was to examine the hypothesis that the extent of pancreatic autophagy is associated with aging and age-related diabetes. Methods: Pancreatic tissue and blood samples were collected from Sprague Dawley rats receiving a normal diet at 2 (the young group), 6 (the adult group), 12 (the middle-age group) and 20-24 (the aged group) months of age. Body weight and fasting blood glucose, serum lipid levels and serum insulin levels were determined. Pancreatic cell structure and autophagy were determined using transmission electron microscopy of rats at 6, 12 and 24 months of age. Lamp2 and LC3b protein expression levels were determined by both immunohistochemistry and Western blot analyses, and islet cell apoptosis was assessed using the TUNEL assay. Results: Fasting blood glucose, triglyceride and FFA levels increased significantly with age (p < 0.05). Compared with levels seen in two-month-old rats, insulin secretion of islet cells in vitro was significantly reduced at 6, 12, and 20 months of age (p < 0.05). Autophagosomes were only observed in islet cells of 24 month-old rats. Increased expression of the autophagic markers, Lamp2 and LC3b, was observed with age. A significant increase in apoptotic index was observed between young rats (two-months-old) and older rats (six-, 12- and 24-months-old), but no differences were observed between rats six, 12 and 24 months of age. Conclusion: Appearance of autophagosomes and increased Lamp2 and LC3b expression in pancreatic islet cells coincided with a significant decrease in insulin secretion and elevation of fasting blood glucose in aged rats.

scholarly journals LIM-Homeodomain Transcription Factor Isl-1 Mediates Kisspeptin's Effect on Insulin Secretion in Mice

2014 ◽  
Vol 28 (8) ◽  
pp. 1276-1290 ◽  
Author(s):  
Juan Chen ◽  
Rui Fu ◽  
Yan Cui ◽  
Jirong Pan ◽  
Yushan Li ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Direct Action ◽  
Janus Kinase ◽  
Homeodomain Transcription Factor ◽  
Lim Homeodomain

Kisspeptin and the G protein-coupled receptor 54 (GPR54) are highly abundant in the pancreas. In addition, circulating kisspeptin directly influences insulin secretion through GPR54. However, the mechanisms by which kisspeptin affects insulin release are unclear. The LIM-homeodomain transcription factor, Isl-1, is expressed in all pancreatic islet cells and is involved in regulating both islet development and insulin secretion. We therefore investigated potential interactions between kisspeptin and Isl-1. Our results demonstrate that Isl-1 and GPR54 are coexpressed in mouse pancreatic islet β-cells and NIT cells. Both in vitro and in vivo results demonstrate that kisspeptin-54 (KISS-54) inhibits Isl-1 expression and insulin secretion and both the in vivo and in vitro effects of KISS-54 on insulin gene expression and secretion are abolished when an Isl-1-inducible knockout model is used. Moreover, our results demonstrate that the direct action of KISS-54 on insulin secretion is mediated by Isl-1. Our results further show that KISS-54 influences Isl-1 expression and insulin secretion through the protein kinase C-ERK1/2 pathway. Conversely, insulin has a feedback loop via the Janus kinase-phosphatidylinositol 3-kinase pathway regulating kisspeptin expression and secretion. These findings are important in understanding mechanisms of insulin secretion and metabolism in diabetes.

scholarly journals TCF7L2 Regulates Late Events in Insulin Secretion From Pancreatic Islet  -Cells

Diabetes ◽  
2009 ◽  
Vol 58 (4) ◽  
pp. 894-905 ◽  
Author(s):  
G. da Silva Xavier ◽  
M. K. Loder ◽  
A. McDonald ◽  
A. I. Tarasov ◽  
R. Carzaniga ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells
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