BROWSE

Related Researcher

Author

Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

ITEM VIEW & DOWNLOAD

Zafirlukast promotes insulin secretion by increasing calcium influx through L-type calcium channels

Cited 0 times inthomson ciCited 0 times inthomson ci
Title
Zafirlukast promotes insulin secretion by increasing calcium influx through L-type calcium channels
Author
Hwang, Hyeon-JeongPark, Kyoung-SuChoi, Jang HyunCocco, LucioJang, Hyun-JunSuh, Pann-Ghill
Keywords
hypoglycemia; insulin secretion; intracellular calcium; L‐ type calcium channels; zafirlukast
Issue Date
201805
Publisher
WILEY-BLACKWELL
Citation
JOURNAL OF CELLULAR PHYSIOLOGY, v., no., pp. -
Abstract
The zafirlukast has been reported to be anti‐inflammatory and widely used to alleviate the symptoms of asthma. However, its influence on insulin secretion in pancreatic β‐cells has not been investigated. Herein, we examined the effects of zafirlukast on insulin secretion and the potential underlying mechanisms. Among the cysteinyl leukotriene receptor 1 antagonists, zafirlukast, pranlukast, and montelukast, only zafirlukast enhanced insulin secretion in a concentration‐dependent manner in both low and high glucose conditions and elevated the level of [Ca2+]i, further activating Ca2+/calmodulin‐dependent protein kinase II (CaMKII), protein kinase B (AKT), and extracellular signal‐regulated kinase (ERK) signaling. These effects were nearly abolished by the L‐type Ca2+ channel antagonist nifedipine, while treatment with thapsigargin, a sarco/endoplasmic reticulum Ca2+ ATPase inhibitor, did not have the same effect, suggesting that zafirlukast primarily induces the entry of extracellular Ca2+ rather than intracellular Ca2+ from the endoplasmic reticulum. Zafirlukast treatment resulting in a significant drop in glucose levels and increased insulin secretion in C57BL/6J mice. These findings will contribute to an improved understanding of the side effects of zafirlukast and potential candidate for a therapeutic intervention in diabetes.
URI
Go to Link
DOI
http://dx.doi.org/10.1002/jcp.26750
ISSN
0021-9541
Appears in Collections:
SLS_Journal Papers
Files in This Item:
There are no files associated with this item.

find_unist can give you direct access to the published full text of this article. (UNISTARs only)

Show full item record

qr_code

  • mendeley

    citeulike

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

MENU