Literature DB >> 27377684

Association of glutathione-S-transferase with patients of type 2 diabetes mellitus with and without nephropathy.

Mohini Sharma1, Stuti Gupta1, Kalpana Singh1, Mohit Mehndiratta1, Amar Gautam2, Om P Kalra2, Rimi Shukla1, Jasvinder K Gambhir3.   

Abstract

STATEMENTS OF THE PROBLEM: Hyperglycemia induced oxidative stress is implicated as a contributor to the onset and progression of type 2 diabetes mellitus (T2DM) and its complications like diabetic nephropathy (DN). Glutathione-S-transferase (GST) is primarily involved in the neutralization of reactive oxygen species (ROS) by enzymatic conjugation with the scavenger peptide glutathione (GSH). Therefore, present study was aimed to evaluate the role of GST along with oxidative stress markers and their correlation in patients with Type 2 diabetes mellitus with and without nephropathy.
METHODS: This study comprised of 300 participants divided into three groups of 100 each: healthy controls (HC), T2DM without complications and DN. Plasma GST, malondialdehyde (MDA), reduced GSH levels and ferric reducing ability of plasma (FRAP) were estimated spectrophotometrically.
RESULTS: Highest GST levels was observed in T2DM which was significantly higher (p<0.05) as compared to DN and HC. However, GSH and FRAP levels were found to be significantly lowest whereas MDA levels were significantly highest in DN as compared to T2DM and HC. GST showed a significant negative correlation with GSH, FRAP and positive correlation with MDA in both patients groups.
CONCLUSIONS: Highest activity of GST in T2DM might be as a compensatory mechanism in response to oxidative stress. GST is found to have significant negative association with decreased GSH. Altered redox milieu in DN collectively conspire to increase the risk of renal damage in T2DM.
Copyright © 2016 Diabetes India. Published by Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Diabetic nephropathy; GSH; GST; Oxidative stress markers; Type 2 diabetes mellitus

Mesh:

Substances:

Year:  2016        PMID: 27377684     DOI: 10.1016/j.dsx.2016.06.006

Source DB:  PubMed          Journal:  Diabetes Metab Syndr        ISSN: 1871-4021


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