Topic
Methylglyoxal
About: Methylglyoxal is a research topic. Over the lifetime, 2844 publications have been published within this topic receiving 102037 citations. The topic is also known as: acetylformaldehyde & pyruvaldehyde.
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TL;DR: It is shown that animals with elevated methylglyoxal recapitulate several core aspects of T2D: insulin resistance, obesity, and hyperglycemia, suggesting that the molecular causes of elevated MG warrant further study.
108 citations
TL;DR: Although there is a close association between methylglyoxal and carbohydrate metabolism, the presence of this 1,2-dicarbonyl in the plasma is mainly due to other mechanisms, and protein glycation and aminoacetone degradation are proposed to be the major and the minor sources of plasma methyl glyoxal under normal conditions.
108 citations
TL;DR: It is demonstrated that mutants lacking the channels can be protected against the lethal effects of methylglyoxal by acidification of the cytoplasm with a weak acid and the implications for pHi‐mediated resistance to methylglyxal are discussed.
Abstract: Escherichia coli possesses two glutathione-gated potassium channels, KefB and KefC, that are activated by glutathione-S-conjugates formed with methylglyoxal. We demonstrate that activation of the channels leads to cytoplasmic acidification and that this protects cells during electrophilic attack. Further, we demonstrate that mutants lacking the channels can be protected against the lethal effects of methylglyoxal by acidification of the cytoplasm with a weak acid. The degree of protection is determined by the absolute value of the pHi and the time at which acidification takes place. Alterations in the pHi do not accelerate the rate of detoxification of methylglyoxal. The mechanism by which methylglyoxal causes cell death and the implications for pHi-mediated resistance to methylglyoxal are discussed.
107 citations
TL;DR: The aim of this mini-review is to assess to what extent MGO is related to vascular complications in diabetes.
Abstract: Various theories have been proposed to explain the hyperglycaemia-induced pathogenesis of vascular complications of diabetes, including detrimental effects of AGEs (advanced glycation end products) on vascular tissues. Increased formation of the very reactive dicarbonyl compound MGO (methylglyoxal), one of the side-products of glycolysis, and MGO-derived AGEs seem to be implicated in the development of diabetic vascular complications. Although the exact role of MGO and MGO adducts in the development of vascular complications is unknown, receptor-mediated activation of vascular cells by the MGO–arginine adduct hydroimidazolone, as well as intracellular modifications of protein by MGO, seem to be involved. The aim of this mini-review is to assess to what extent MGO is related to vascular complications in diabetes.
107 citations
TL;DR: The induction of HB-EGF by MG and 3-DG, as well as the concomitant increment of intracellular peroxides, may trigger atherogenesis during diabetes.
107 citations