Dicarbonyls and Advanced Glycation End-Products in the Development of Diabetic Complications and Targets for Intervention.

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Term Occurence Count Dictionary
diabetic neuropathy 5 endocrinologydiseases
diabetic retinopathy 3 endocrinologydiseases
metformin 8 endocrinologydiseasesdrugs
trientine 1 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
metformin 36889 sufficient for MG binding in vivo another hurdle in diabetic patients would be competition for binding with metformin . The latter compound is the current first-line therapy for type 2 diabetes and reacts covalently with
metformin 37191 treatment of choice for type 2 diabetes due to its glucose lowering effect [[134]]. MG lowering effects of metformin have been reported in addition [[158]]. The mechanism behind the decrease in MG levels by metformin
metformin 37291 metformin have been reported in addition [[158]]. The mechanism behind the decrease in MG levels by metformin is uncertain. Metformin reacts with MG via its guanidine group but the reaction proceeds slowly [[159]].
metformin 37425 reacts with MG via its guanidine group but the reaction proceeds slowly [[159]]. Nevertheless, a MG- metformin adduct has been detected in urine of patients treated with the drug at concentrations up to 4.3 μM
metformin 37569 of patients treated with the drug at concentrations up to 4.3 μM [[156]]. Lowering of MG levels by metformin is associated with an increase of GLO1 in peripheral blood mononuclear cells and a trend for increase
metformin 37714 GLO1 in peripheral blood mononuclear cells and a trend for increase in red blood cells [[160]]. Thus metformin may inhibit AGE formation directly through lowering of MG levels via two ways, namely MG scavenging
metformin 43765 strongly associated with the development of complications. One reason for the therapeutic success of metformin may be that it interferes with dicarbonyl and AGE formation on several levels, namely by lowering blood
metformin 44122 lowering dicarbonyls and AGE formation must be better at scavenging dicarbonyls or inducing GLO1 than metformin . Furthermore, alternative pathways for the reduction of AGE formation, such as transition metal chelation
trientine 40316 not measured [[174],[175]]. In another phase 2 clinical trial, administration of the copper chelator trientine over one year partially restored left ventricular hypertrophy in diabetic patients [[176]]. 7.3. Future
Select Disease Character Offset Disease Term Instance
diabetic neuropathy 14636 It was found that skin levels of AGEs are associated with the progression of diabetic nephropathy, diabetic neuropathy and diabetic retinopathy in type 1 diabetic humans [[3]]. Interestingly, in this study the correlation
diabetic neuropathy 14793 diabetic humans [[3]]. Interestingly, in this study the correlation of MG-H1, with the development of diabetic neuropathy was very strong even when corrected for all other risk factors. This provides support for the finding
diabetic neuropathy 15217 correlated with the heat pain detection threshold in the foot further confirming the importance of MG in diabetic neuropathy [[71]]. However, another recent study found no correlation between serum MG levels and peripheral neuropathy
diabetic neuropathy 15467 patients [[72]]. As the authors commented this does not rule out a role for MG in the pathogenesis of diabetic neuropathy . Levels of the MG-derived AGE MG-H1 are extraordinarily high in the sciatic nerve so that MG plasma
diabetic neuropathy 20553 [[3],[39],[41]]. In line with these findings no correlation of G-H1 skin levels with diabetic nephropathy, diabetic neuropathy and diabetic retinopathy were seen [[3]]. In contrast the glyoxal-derived DNA adduct GdG was strongly
diabetic retinopathy 14660 levels of AGEs are associated with the progression of diabetic nephropathy, diabetic neuropathy and diabetic retinopathy in type 1 diabetic humans [[3]]. Interestingly, in this study the correlation of MG-H1, with the development
diabetic retinopathy 20577 these findings no correlation of G-H1 skin levels with diabetic nephropathy, diabetic neuropathy and diabetic retinopathy were seen [[3]]. In contrast the glyoxal-derived DNA adduct GdG was strongly elevated in plasma of diabetic
diabetic retinopathy 34684 was seen in another study [[138],[139],[140]]. Positive effects of aminoguanidine were also seen on diabetic retinopathy [[141]]. While preclinical studies were promising overall, clinical trials of the compound were disappointing.

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