uu.seUppsala University Publications
Change search
ReferencesLink to record
Permanent link

Direct link
Metabolic stress in insulin's target cells leads to ROS accumulation - a hypothetical common pathway causing insulin resistance.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Endocrinology, Diabetes and Metabolism.
2007 (English)In: FEBS Letters, ISSN 0014-5793, E-ISSN 1873-3468, Vol. 581, no 19, 3734-42 p.Article in journal (Refereed) Published
Abstract [en]

The metabolic syndrome is a cluster of cardiovascular risk factors, and visceral adiposity is a central component that is also strongly associated with insulin resistance. Both visceral obesity and insulin resistance are important risk factors for the development of type 2 diabetes. It is likely that adipose tissue, particularly in the intra-abdominal depot, is part of a complex interplay involving several tissues and that dysregulated hormonal, metabolic and neural signalling within and between organs can trigger development of metabolic disease. One attractive hypothesis is that many factors leading to insulin resistance are mediated via the generation of abnormal amounts of reactive oxygen species (ROS). There is much evidence supporting that detrimental effects of glucose, fatty acids, hormones and cytokines leading to insulin resistance can be exerted via such a common pathway. This review paper mainly focuses on metabolic and other 'stress' factors that affect insulin's target cells, in particular adipocytes, and it will highlight oxidative stress as a potential unifying mechanism by which these stress factors promote insulin resistance and the development and progression of type 2 diabetes.

Place, publisher, year, edition, pages
2007. Vol. 581, no 19, 3734-42 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-211262DOI: 10.1016/j.febslet.2007.06.044PubMedID: 17628546OAI: oai:DiVA.org:uu-211262DiVA: diva2:681628
Available from: 2013-12-20 Created: 2013-11-21 Last updated: 2013-12-20

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed
By organisation
Endocrinology, Diabetes and Metabolism
In the same journal
FEBS Letters
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 144 hits
ReferencesLink to record
Permanent link

Direct link