Tangvarasittichai S. Oxidative stress, insulin resistance, dyslipidemia and type 2 diabetes mellitus. World J Diabetes 2015; 6(3): 456-480 [PMID: 25897356 DOI: 10.4239/wjd.v6.i3.456]
Corresponding Author of This Article
Dr. Surapon Tangvarasittichai, Associate Professor, Chronic Disease Research Unit, Department of Medical Technology, Faculty of Allied Health Sciences, Naresuan University, 99 Moo 9 Tambon Tha Pho, Muang, Phitsanulok 65000, Thailand. surapon14t@yahoo.com
Research Domain of This Article
Cell Biology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Apr 15, 2015; 6(3): 456-480 Published online Apr 15, 2015. doi: 10.4239/wjd.v6.i3.456
Oxidative stress, insulin resistance, dyslipidemia and type 2 diabetes mellitus
Surapon Tangvarasittichai
Surapon Tangvarasittichai, Chronic Disease Research Unit, Department of Medical Technology, Faculty of Allied Health Sciences, Naresuan University, Phitsanulok 65000, Thailand
Author contributions: Tangvarasittichai S and his assistances performed the literatures review search and wrote the manuscript; Tangvarasittichai S designed essential ideas, drawing figures and sequencing of this review manuscript, also provided references and edited the manuscript, addressed the responses to reviewers’ concerns and contributed to the edition of the manuscript.
Conflict-of-interest: The author declares that there are no conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Surapon Tangvarasittichai, Associate Professor, Chronic Disease Research Unit, Department of Medical Technology, Faculty of Allied Health Sciences, Naresuan University, 99 Moo 9 Tambon Tha Pho, Muang, Phitsanulok 65000, Thailand. surapon14t@yahoo.com
Telephone: +66-08-96388382 Fax: +66-08-55966300
Received: September 3, 2014 Peer-review started: September 4, 2014 First decision: November 14, 2014 Revised: December 25, 2014 Accepted: January 9, 2015 Article in press: January 12, 2015 Published online: April 15, 2015
Abstract
Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus (T2DM) and this appears to underlie the development of cardiovascular disease, T2DM and diabetic complications. Increased oxidative stress appears to be a deleterious factor leading to insulin resistance, dyslipidemia, β-cell dysfunction, impaired glucose tolerance and ultimately leading to T2DM. Chronic oxidative stress, hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant, have high oxidative energy requirements, decrease the gene expression of key β-cell genes and induce cell death. If β-cell functioning is impaired, it results in an under production of insulin, impairs glucose stimulated insulin secretion, fasting hyperglycemia and eventually the development of T2DM.
Core tip: Oxidative stress is underling in the development of cardiovascular disease, type 2 diabetes mellitus (T2DM) and diabetic complications. Increased oxidative stress appears to be a deleterious factor leading to insulin resistance, dyslipidemia, β-cell dysfunction, impaired glucose tolerance and ultimately leading to T2DM.
