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: 4(5)-Methylimidazole has received the attention of federal and state regulatory agencies because of its carcinogenicity and common presence in foods and beverages and a methylglyoxal/NH(3) system produced significantly higher levels of 4- or 5-methylimIDazole, suggesting that methyl Glyoxal is an important precursor of 4( 5)-methy Limidazoles.
Abstract: 4(5)-Methylimidazole has received the attention of federal and state regulatory agencies because of its carcinogenicity and common presence in foods and beverages. In the present study, the formation of 4(5)-methylimidazole in Maillard reaction model systems consisting of d-glucose/NH3, l-rhamnose/NH3, methylglyoxal/NH3, and methylglyoxal/formaldehyde/NH3 was investigated. 4(5)-Methylimidazole was formed at levels ranging from 0.49 to 0.71 mg/mL in the d-glucose/NH3 model system. The formation of 4(5)-methylimidazole was slightly higher in the l-rhamnose/NH3 system (0.91 mg/mL) than in the d-glucose/NH3 system (0.71 mg/mL) under the conditions used in the present study. A methylglyoxal/NH3 system produced significantly higher levels of 4(5)-methylimidazole (5.70 mg/mL), suggesting that methylglyoxal is an important precursor of 4(5)-methylimidazole. Ammonolysis of methylglyoxal, which is one of the glucose degradation products, was proposed to form formamide, which subsequently reacted with 2-aminopropana...
99 citations
TL;DR: Aldose reductase–catalyzed reduction is an important pathway in the endothelial and cardiac metabolism of AGE precursors, and it prevents AGE accumulation and atherosclerotic lesion formation.
Abstract: Objective: To examine the role of aldo-keto reductases (AKRs) in the cardiovascular metabolism of the precursors of advanced glycation end products (AGEs). Research Design and Methods: Steady-state kinetic parameters of AKRs with AGE precursors were determined using recombinant proteins expressed in bacteria. Metabolism of methylglyoxal and AGE accumulation were studied in human umbilical vein endothelial cells (HUVECs), C57-wild-type, akr1b3 (aldose reductase, AR)-null and cardiospecific akr1b4 (rat AR) and akr1b8 -(FR-1) transgenic mice. AGE accumulation and atherosclerotic lesions were studied 12 weeks after streptozotocin-treatment of C57, akr1b3 -null, and apoE - and akr1b3 - apoE -null mice. Results: Higher levels of AGEs were generated in the cytosol than at the external surface of HUVECs cultured in high glucose, indicating that intracellular metabolism may be an important regulator of AGE accumulation and toxicity. In vitro , AKR 1A and 1B catalyzed the reduction of AGE precursors, whereas AKR1C, AKR6, and AKR7 were relatively ineffective. Highest catalytic efficiency was observed with AKR1B1. Acetol formation in methylglyoxal-treated HUVECs was prevented by the AR inhibitor sorbinil. Acetol was generated in hearts perfused with methylglyoxal and its formation was increased in akr1b4 - or akr1b8 -transgenic mice. Reduction of AGE precursors was diminished in hearts from akr1b3 -null mice. Diabetic akr1b3 -null mice accumulated more AGEs in the plasma and the heart than WT mice and deletion of akr1b3 increased AGE accumulation and atherosclerotic lesion formation in apoE -null mice. Conclusion: Aldose reductase-catalyzed reduction is an important pathway in the endothelial and cardiac metabolism of AGE precursors and it prevents AGE accumulation and atherosclerotic lesion formation.
99 citations
TL;DR: A potential role for MG is suggested in SC injury through oxidative stress-mediated p38 MAPK activation under diabetic conditions, and it may serve as a novel insight into therapeutic strategies for diabetic neuropathy.
98 citations
TL;DR: Methylglyoxal binds and irreversibly modifies arginine and lysine residues in bovine serum albumin under physiological conditions, producing a protein with an increased net negative charge at physiological pH.
98 citations
TL;DR: MGO participates not only in the pathogenesis of the debilitating complications of type 2 diabetes, but also in worsening of the diabetic state by favouring beta cell failure.
Abstract: Aims/hypothesis
Chronic hyperglycaemia aggravates insulin resistance, at least in part, by increasing the formation of advanced glycation end-products (AGEs). Methylglyoxal (MGO) is the most reactive AGE precursor and its abnormal accumulation participates in damage in various tissues and organs. Here we investigated the ability of MGO to interfere with insulin signalling and to affect beta cell functions in the INS-1E beta cell line.
98 citations