Short-term very low calory diet reduces oxidative stress in obese type 2 diabetic patients

Title:

Short-term very low calory diet reduces oxidative stress in obese type 2 diabetic patients

Creator:

Škrha, J., Kunešová, M., Hilgertová, J., Weiserová, H., Křížová, J., and Kotrlíková, E.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:cabb3a00-9302-4be2-93a1-60c44ed2c93d
uuid:cabb3a00-9302-4be2-93a1-60c44ed2c93d

Subject:

Oxidative stress, Very low calory diet, Obesity, and Type 2 diabetes mellitus

Type:

article, model:article, and TEXT

Description:

In addition to a number of deleterious effects on cellular integrity and functions, diabetic metabolic milieu has been implicated in a rapidly growing number of alterations in signal transduction. In this review we focus on Akt kinase physiology, its alterations in diabetes mellitus (DM), and on the emerging role of this signaling system in the pathophysiology of diabetic microvascular complications. Studies focusing on Akt in diabetes suggest both decrease and increase of Akt activity in DM. Alterations of Akt activity have been found in various tissues and cells in diabetes depending on experimental and clinical contexts. There is convincing evidence suggesting defective Akt signaling in the development of insulin resistance. Similar defects, as in insulin-sensitive tissues, have been reported in endothelia of DM Type 2 models, possibly contributing to the development of endothelial dysfunction under these conditions. In contrast, Akt activity is increased in some tissues and va scular beds affected by complications in DM Type 1. Identification of the role of this phenomenon in DM-induced growth and hemodynamic alterations in affected vascular beds remains one of the major challenges for future research in this area. Future studies should include the evaluation of therapeutical benefits of pharmacological modulators of Akt activity.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2005 Volume:54 | Number:1

Harvested from:

CDK

Metadata only:

false