Add like
Add dislike
Add to saved papers

Does Glycemic Control Modulate the Impairment of NLRP3 Inflammasome Activation in Type 2 Diabetes?

Since mitochondrial dysfunction is associated with NOD-like receptor family protein 3 (NLRP3) activation in type 2 diabetes (T2D), which can eventually lead to an impaired immune response, we set out to determine if glycemic control modulates the effects of T2D on the NLRP3 inflammasome. We have studied leukocytes from 61 diabetic patients [25 with glycated hemoglobin (HbA1c ) ≤7% and 36 with HbA1c ≥8%] and 40 healthy controls. Total and mitochondrial reactive oxygen species (ROS) production was enhanced in T2D patients, and mitochondrial ROS was more pronounced in those with poor glycemic control. Levels of gene and protein expression of NLRP3 were decreased in both diabetic groups and more so in those with HbA1c ≥8%. In addition, there was a decrease in gene expression and serum concentrations of interleukin (IL)-1β, IL-12, and caspase-1 in line with inhibition of the NLRP3 inflammasome. Our data also suggest negative correlations between HbA1c levels and NLRP3 protein expression, serum levels of IL-12 and IL-1β, and caspase-1 messenger RNA expression. Our findings lead us to raise the hypothesis of an association between poor glycemic control in T2D and an impairment of the NLRP3 inflammasome, suggesting that glycemic control plays an important role in the immune response of diabetic subjects. Antioxid. Redox Signal. 00, 000-000.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app