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Journal ArticleDOI

Proinflammatory and proapoptotic effects of methylglyoxal on neutrophils from patients with type 2 diabetes mellitus.

TLDR
MG stimulated neutrophils to release more cytokines, which might play a role in the development of infection in T2DM, which was correlated positively with glycated hemoglobin levels, fasting plasma glucose levels and urine albumin/creatinine ratios.
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This article is published in Clinical Biochemistry.The article was published on 2007-11-01. It has received 131 citations till now. The article focuses on the topics: Proinflammatory cytokine & Cytokine.

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Journal ArticleDOI

Oxidative stress and aging: is methylglyoxal the hidden enemy?

TL;DR: The potential role of MG in the aging process through increasing oxidative stress besides causing AGEs formation is discussed and specific and effective scavengers and crosslink breakers of MG and A GEs are being developed and can become potential treatments to slow the Aging process and prevent many diseases.
Journal ArticleDOI

Methylglyoxal promotes oxidative stress and endothelial dysfunction

TL;DR: Evidence is provided for methylglyoxal as one of the causative factors in the pathogenesis of atherosclerosis and development of macrovascular diabetic complication by increasing oxidative stress and/or AGEs formation with a concomitant increment of inflammation and a decrement in NO bioavailability.
Journal ArticleDOI

The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System.

TL;DR: The focus of the current review is to explore metabolic and immunological abnormalities affecting several organs of T2DM patients and explain the mechanisms, whereby diabetic patients become more susceptible to infectious diseases.
Journal ArticleDOI

A “Turn-On” Fluorescent Sensor for Methylglyoxal

TL;DR: It is shown that MBo is selective for MGO over other biologically relevant dicarbonyls and is suitable for detecting MGO in complex environments, including that of living cells, and its utility in estimating plasma concentrations of MGO is demonstrated.
Journal ArticleDOI

Chronic Methylglyoxal Infusion by Minipump Causes Pancreatic β-Cell Dysfunction and Induces Type 2 Diabetes in Sprague-Dawley Rats

TL;DR: Investigating the effects of chronic administration of MG on glucose tolerance and β-cell insulin secreting mechanism in 12-week-old male Sprague-Dawley rats found it induces biochemical and molecular abnormalities characteristic of type 2 diabetes and is a possible mediator of high carbohydrate-induced type 1 diabetes.
References
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Journal Article

Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)

R C Turner, +398 more
- 12 Sep 1998 - 
TL;DR: In this article, the effects of intensive blood-glucose control with either sulphonylurea or insulin and conventional treatment on the risk of microvascular and macrovascular complications in patients with type 2 diabetes in a randomised controlled trial were compared.
Journal ArticleDOI

Nuclear factor-kappaB: a pivotal transcription factor in chronic inflammatory diseases.

TL;DR: In chronic inflammatory diseases, such as asthma, rheumatoid arthritis, inflammatory bowel disease, and psoriasis, several cytokines recruit activated immune and inflammatory cells to the site of lesions, thereby amplifying and perpetuating the inflammatory state.
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Immune dysfunction in patients with diabetes mellitus (DM)

TL;DR: Patients with diabetes mellitus (DM) have infections more often than those without DM and an increased adherence of microorganisms to diabetic compared to nondiabetic cells has been described for Candida albicans.
Journal ArticleDOI

Impaired leucocyte functions in diabetic patients.

TL;DR: All steps of PMN functioning are altered in diabetic patients, which may increase the risk of vascular complications and infectious episodes.
Journal ArticleDOI

Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy

TL;DR: In diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury, and Restriction of dietary A GEs suppresses these effects.
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