Short-term glucose variability in healthy volunteers is not associated with raised oxidative stress markers

2012 ◽  
Vol 14 (11) ◽  
pp. 1047-1049 ◽  
Author(s):  
A. Wakil ◽  
K. A. Smith ◽  
S. L. Atkin ◽  
E. S. Kilpatrick
2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Hazal Tuzcu ◽  
Ibrahim Aslan ◽  
Mutay Aslan

Effect of high-dose insulin analog initiation therapy was evaluated on lipid peroxidation and oxidative stress markers in type 2 diabetes mellitus (T2DM). Twenty-four T2DM patients with HbA1c levels above 10% despite ongoing therapy with sulphonylurea and metformin were selected. Former treatment regimen was continued for the first day followed by substitution of sulphonylurea therapy with different insulin analogs. Glycemic profiles were determined over 72 hours by Continuous Glucose Monitoring System (CGMS), and blood/urine samples were collected at 24 and 72 hours. Insulin analog plus metformin treatment significantly reduced glucose variability. Plasma and urine lipid peroxidation were markedly decreased following insulin analog plus metformin treatment. No correlation existed between glucose variability and levels of plasma and urine oxidative stress markers. Likewise, changes in mean blood glucose from baseline to end point showed no significant correlation with changes in markers of oxidative stress. On the contrary, decreased levels of oxidative stress markers following treatment with insulin analogs were significantly correlated with mean blood glucose levels. In conclusion, insulin plus metformin resulted in a significant reduction in oxidative stress markers compared with oral hypoglycemic agents alone. Data from this study suggests that insulin analogs irrespective of changes in blood glucose exert inhibitory effects on free radical formation.


2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii509-iii509
Author(s):  
Raymond Pratt ◽  
Dorine Swinkels ◽  
T. Alp Ikizler ◽  
Carrrie Guss ◽  
Vivian Lin ◽  
...  

2015 ◽  
Vol 14 (2) ◽  
pp. 211-218 ◽  
Author(s):  
Marianne Skov ◽  
Tacjana Pressler ◽  
Jens Lykkesfeldt ◽  
Henrik Enghusen Poulsen ◽  
Peter Østrup Jensen ◽  
...  

2016 ◽  
Vol 28 (4) ◽  
pp. 222-228 ◽  
Author(s):  
Christopher Didigwu Nwani ◽  
Gregory Ejike Odo ◽  
Alfreda O. Nwadinigwe ◽  
Christopher C. Onyeke ◽  
Chinedu Ifeanyi Atama ◽  
...  

2019 ◽  
Vol 51 (Supplement) ◽  
pp. 88
Author(s):  
Majid S. Koozehchian ◽  
Khadijeh Taheri Kazaj ◽  
Amir Sarshin ◽  
Abbasali Gaeini ◽  
Alireza Naderi ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1018
Author(s):  
Dominika Kanikowska ◽  
Alina Kanikowska ◽  
Ewelina Swora-Cwynar ◽  
Marian Grzymisławski ◽  
Maki Sato ◽  
...  

Oxidative stress and inflammation are implicated in obesity. Therefore, we investigated whether moderate and short-term calorie restriction (CR) reflects a real-life situation, mediates weight loss, and improves oxidative stress markers. We analyzed oxidative stress markers in patients with obesity undergoing moderate CR. Serum oxidative stress markers (myeloperoxidase (MPO), superoxide dismutase (SOD), catalase, total antioxidant status (TAS), and reactive oxygen species (ROS) (generation by endothelial cells in vitro)) were measured in 53 subjects (mean BMI 37.8 ± 5.9 kg/m2) who underwent 8 weeks of CR, which included a reduction of 300–500 kcal/day. MPO was the most CR-sensitive parameter. The mean level of serum MPO in patients with obesity was 20% higher than that in post CR intervention (p < 0.001). SOD increased by 12% after CR (p < 0.05), which was largely due to the improvement in glucose tolerance and the reduction in insulin resistance after CR. Other tested parameters were not modified during the treatment. CR resulted in an expected decrease in body weight (by 5.9 ± 4.6 kg, p < 0.0001) and other anthropometric parameters. Additionally, it was accompanied by a significant change in hsCRP, hsTNF alpha, hsIL-6, leptin (all p < 0.0001), and HOMA-IR (p < 0.05). Cardiovascular and metabolic parameters were also partially improved. Short-term, moderate CR partially improves antioxidant capacity but is enough to substantially change anthropometric parameters in obese patients. Our observations indicate that mimicking real-life situations and low-cost dietary intervention can be successfully implemented in obesity treatment with a simultaneous moderate effect on antioxidant status.


Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 765
Author(s):  
Dominika Stygar ◽  
Aleksandra Pogorzelska ◽  
Elżbieta Chełmecka ◽  
Bronisława Skrzep-Poloczek ◽  
Barbara Bażanów ◽  
...  

Since biological applications and toxicity of graphene-based materials are structure dependent, studying their interactions with the biological systems is very timely and important. We studied short-term (1, 24, and 48 h) effects of ultrapure (GO) and Mn2+-contaminated (GOS) graphene oxide on normal human dermal fibroblasts (NHDF) and adenocarcinomic human alveolar basal epithelial cells (A549) using selected oxidative stress markers and cytokines: glutathione reductase (GR) and catalase (CAT) activity, total antioxidative capacity (TAC), and malondialdehyde (MDA) concentration, levels of vascular endothelial growing factor (VEGF), tumor necrosis factor-alpha (TNF-a), platelet-derived growth factor-BB (PDGF-BB), and eotaxin. GOS induced higher levels of oxidative stress, measured with CAT activity, TAC, and MDA concentration than GO in both cell lines when compared to control cells. GR activity decreased in time in NHDF cells but increased in A549 cells. The levels of cytokines were related to the exposure time and graphene oxide type in both analyzed cell lines and their levels comparably increased over time. We observed higher TNF-a levels in NHDF and higher levels of VEGF and eotaxin in the A549 cell line. Both types of cells showed similar susceptibility to GO and GOS. We concluded that the short-time exposure to GOS induced the stronger response of oxidative stress markers without collapsing the antioxidative systems of analysed cells. Increased levels of inflammatory cytokines after GO and GOS exposure were similar both in NHDF and A549 cells.


Sign in / Sign up

Export Citation Format

Share Document