Effects of gestational and overt diabetes on placental cytochromes P450 and glutathione S-transferase

Glover, Douglas D.; McRobie, Donna J.; Tracy, Timothy S.

doi:10.1016/s1068-607x(98)00111-5

Cited by 7 publications

(2 citation statements)

References 36 publications

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“…Both acrylamide and NDMA are metabolically activated into genotoxic metabolites by CYP2E1 [155,156]. Our results [25,110,111] agree with the fact that CYP2E1 activity necessary for acrylamide activation is very low or non‐existent in human placentas [157–159], although there is some indication that CYP2E1 could be active in the placentas of mothers consuming large amounts of alcohol [160]. Also, mRNA of CYP2E1 has been found in human placentas [89,161,162].…”

Section: Placental Metabolism and Dna Adduct Formationsupporting

confidence: 83%

Foetal Exposure to Food and Environmental Carcinogens in Human Beings

Myöhänen

Vähäkangas

2011

Basic Clin Pharma Tox

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Section: Placental Metabolism and Dna Adduct Formationsupporting

confidence: 83%

Foetal Exposure to Food and Environmental Carcinogens in Human Beings

Myöhänen

Vähäkangas

2011

Basic Clin Pharma Tox

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“…cin-induced diabetic rats (31), and in the placenta of overt diabetic patients (32). Reactive intermediates generated through metabolism are detoxicated by several systems.…”

Section: Fig 2 Silver-stained Mouse Islet Of Langerhans 2-de Imagementioning

confidence: 99%

Effect of Rosiglitazone on the Differential Expression of Diabetes-associated Proteins in Pancreatic Islets of C57Bl/6 lep/lep Mice

Sanchez

Converset

Nolan

et al. 2002

Molecular & Cellular Proteomics

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The insulin sensitizer drug, rosiglitazone, has been shown to have a protective effect on pancreatic islet cell structure and function in animal models of type 2 diabetes. The identification of new molecular targets associated both with islet cell dysfunction and protection is a crucial research goal. In the present study, a proteomics approach has been used to identify such targets. Obese C57Bl/6J lep/lep mice and lean littermates were given the insulin sensitizer drug BRL49653, rosiglitazone. It normalized the impaired glucose tolerance in lep/lep mice but had no significant effect on glucose tolerance in the lean mice. Pancreatic islet polypeptides were arrayed by a two-dimensional gel electrophoresis system that separated more than 2500 individual spots. Three overexpressed and six underexpressed proteins were significant (p < 0.05) between lep/lep and lean mice, and four were modulated significantly (p < 0.05) by the rosiglitazone treatment of the obese mice. The identity of these differentially expressed proteins was made using mass spectrometric analysis and provided evidence that differential expression of actin-binding proteins may be an important aspect of defective islet function. Rosiglitazone increased carboxypeptidase B expression in both lep/lep and normal mice suggesting that this might be an independent effect of rosiglitazone that contributes to improved insulin processing.

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