Mechanistic studies of advanced glycosylation end product inhibition by aminoguanidine

Edelstein, D.; Brownlee, Michael

doi:10.2337/diabetes.41.1.26

Cited by 126 publications

(64 citation statements)

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“…Second, to propose the mechanism of action of aminoguanidine to be the inhibition of NOS, it should be demonstrated that nitric oxide metabolites are lower in treated animals. Aminoguanidine not only inhibits NO synthase, but has several other effects, such as inhibition of copper-containing amino oxidases [34], inhibition of nonenzymatic formation of advanced glycosylation products [34,35,36], inhibition of histamine metabolism [37], inhibition of polyamine catabolism [38], and inhibition of catalase [34]. Whether one or several of these effects is involved in the changes observed in this study is unknown.…”

Section: Discussionmentioning

confidence: 77%

Hemodynamic, biochemical and morphological changes induced by aminoguanidine in normal and septic sheep

et al. 2000

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Section: Discussionmentioning

confidence: 77%

Hemodynamic, biochemical and morphological changes induced by aminoguanidine in normal and septic sheep

et al. 2000

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“…Aminoguanidine inhibits the formation of AGEs [108] and has beneficial effects on the development of retinopathy, nephropathy and neuropathy. NCV slowing and myelinated fiber pathology in the STZ rat are improved after long-term treatment with aminoguanidine [109].…”

Section: Non-enzymatic Glycation and Oxidative Stressmentioning

confidence: 99%

New insights into the metabolic and molecular basis for diabetic neuropathy

Sima

2003

Cellular and Molecular Life Sciences (CMLS)

150

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Diabetic polyneuropathy is the most common complication of diabetes mellitus. Several interactive pathogenetic mechanisms have been identified mainly in streptozotocin-induced diabetes in rats and have been ascribed to hyperglycemia. Over the last number of years it is becoming increasingly clear that diabetic neuropathy differs in type 1 and type 2 diabetes in humans and in murine models that more accurately mimic the human disorders. Beside hyperglycemia, attention is increasingly being paid to the pathogenetic roles of insulin and C-peptide deficiencies, particularly in type 1 diabetic neuropathy. There is now evidence to suggest that insulin and C-peptide deficiencies are mainly responsible for perturbations of neurotrophic factors and contribute to oxidative stress in diabetic nerve. This may also be true for apoptotic phenomena afflicting both the peripheral and central nervous systems in diabetes. The new data have lead to re-evaluations of pathogenetic components in this complex disorder, and their further exploration is likely to form a more refined basis for future therapeutic and preventive measures.

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“…4). In a later study evidence was presented showing that AMG primarily acts by reacting with Amadori reaction products such as 3-deoxyglucosone [52]. AMG inhibits the formation of AGEs not only in vitro but also in vivo.…”

Section: Inhibition Of Formation Of Advanced Glycosylation End Producmentioning

confidence: 99%

“…Aminoguanidine (AMG) inhibits the formation of intermediate metabolites down-stream to Amadori products. For further information see Brownlee et al[3] and Edelstein and Brownlee[52].…”

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confidence: 99%

Biological effects of aminoguanidine: An update

Nilsson¹

1999

Inflammation Research

193

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Aminoguanidine (AMG) was prepared more than 100 years ago. During the last 10 years two important effects of AMG have been discovered which have made this molecule attract a lot of interest. Firstly, AMG inhibits, in vitro and in vivo, formation of highly reactive advanced glycosylation end products (AGEs) associated with pathogenesis of secondary complications to diabetes and with cardiovascular changes in aging. AMG ameliorates various complications to diabetes and prevents age related arterial stiffening and cardiac hypertrophy, effects probably dependent on inhibition of AGEs formation. Secondly, AMG inhibits NO synthase particularly the inducible NO synthase isoform making AMG an important pharmacological tool. The inducible NO synthase isoform is associated with production of large quantities of NO synthase in response to e. g. cytokines. When these effects of AMG were disclosed it had already been known for many years that AMG, in nM concentrations, inhibits diamine oxidase. This enzyme catalyzes degradation of biologically active diamines such as histamine and putrescine. Data obtained from studies using AMG should be interpreted with precaution since this substance interferes with several important regulatory systems. In this review these important targets for AMG are addressed.

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Mechanistic studies of advanced glycosylation end product inhibition by aminoguanidine

Cited by 126 publications

References 0 publications

Hemodynamic, biochemical and morphological changes induced by aminoguanidine in normal and septic sheep

Hemodynamic, biochemical and morphological changes induced by aminoguanidine in normal and septic sheep

New insights into the metabolic and molecular basis for diabetic neuropathy

Biological effects of aminoguanidine: An update

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