Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2009 Dec;52(12):2489-98.
doi: 10.1007/s00125-009-1536-z. Epub 2009 Oct 7.

Insights into the critical role of NADPH oxidase(s) in the normal and dysregulated pancreatic beta cell

P Newsholme  1 , D Morgan, E Rebelato, H C Oliveira-Emilio, J Procopio, R Curi, A Carpinelli
Affiliations
Review

Insights into the critical role of NADPH oxidase(s) in the normal and dysregulated pancreatic beta cell

P Newsholme et al. Diabetologia. 2009 Dec.

Abstract

It is now widely accepted that reactive oxygen species (ROS) contribute to cell and tissue dysfunction and damage in diabetes. The source of ROS in the insulin secreting pancreatic beta cells has traditionally been considered to be the mitochondrial electron transport chain. While this source is undoubtedly important, we fully describe in this article recent information and evidence of NADPH oxidase-dependent generation of ROS in pancreatic beta cells and identify the various isoforms that contribute to O(2)(*-) and H(2)O(2) production in various conditions. While glucose-stimulated ROS generation may be important for acute regulation of insulin secretion, at higher levels ROS may disrupt mitochondrial energy metabolism. However, ROS may alter other cellular processes such as signal transduction, ion fluxes and/or cell proliferation/death. The various beta cell isoforms of NADPH oxidase (described in this review) may, via differences in the kinetics and species of ROS generated, positively and negatively regulate insulin secretion and cell survival.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Diabetes. 1988 Nov;37(11):1453-69 - PubMed
    1. J Biol Chem. 1984 Jan 10;259(1):47-52 - PubMed
    1. Biochem Biophys Res Commun. 2003 Jan 3;300(1):216-22 - PubMed
    1. Diabetes. 2000 Jul;49(7):1123-30 - PubMed
    1. Cell Signal. 2006 Jan;18(1):69-82 - PubMed

Publication types

LinkOut - more resources