論文

査読有り
2008年11月

Effect of the organophosphorus pesticide diazinon on glucose tolerance in type 2 diabetic rats

TOXICOLOGY LETTERS
  • Jun Ueyama
  • Michihiro Kamijima
  • Kazumi Asai
  • Aiko Mochizuki
  • Dong Wang
  • Takaaki Kondo
  • Toshiaki Suzuki
  • Kenji Takagi
  • Kenzo Takagi
  • Hiroaki Kanazawa
  • Ken-ichi Miyamoto
  • Shinya Wakusawa
  • Takaaki Hasegawa
  • 全て表示

182
1-3
開始ページ
42
終了ページ
47
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.toxlet.2008.08.004
出版者・発行元
ELSEVIER IRELAND LTD

We have reported that the toxicity of the organophosphorus pesticide diazinon (DZN) and its metabolites is increased in streptozotocin-induced diabetic rats (type I diabetic rats). In the present study, we have investigated the effect of DZN on glucose tolerance in genetic type 2 diabetic rats, Goto-Kakizaki (GK) rats. Oral glucose tolerance test (OGTT) (2g/(5 ml kg)) was assessed before, and I and 2 weeks after intraperitoneal injection of DZN (6.5 mg/kg)in Wistar and GK rats. DZN significantly increased the levels of glucose in plasma at designated blood sampling points in GK rats. The activity of hepatic drug-metabolizing enzymes and expression of hepatic cytochrome P450 (CYP) 1A2, CYP3A2 and CYP2D1, which oxidize DZN to DZN-oxon, a potent ChE inhibitor, were measured before DZN injection. There were no significant differences in the activity and expression of CYPs between both rat groups, indicating that the ability of metabolic activation might be almost the same in Wistar and GK rats. DZN dramatically decreased the activity of cholinesterase (ChE) in plasma by approximately 40% in both Wistar and GK rats. However, no significant differences in the activity of ChE in plasma were observed between Wistar and GK rats for 5 days after DZN injection. No massive necrotic and apoptotic areas, leukocyte infiltration and immunoreactive insulin-positive cells (P-cells) were observed in pancreas 2 weeks after DZN injection. Moreover, DZN might not affect plasma insulin levels in Wistar and GK Fats. These results suggest that DZN deteriorates the glucose tolerance in GK Fats. It is unlikely that this phenomenon is due to differences in ChE activity and/or DZN-oxon production levels between Wistar and GK rats. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.toxlet.2008.08.004
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000261285800007&DestApp=WOS_CPL
URL
http://www.scopus.com/inward/record.url?eid=2-s2.0-54949091463&partnerID=MN8TOARS
URL
http://orcid.org/0000-0003-0660-2726
ID情報
  • DOI : 10.1016/j.toxlet.2008.08.004
  • ISSN : 0378-4274
  • ORCIDのPut Code : 47185914
  • SCOPUS ID : 54949091463
  • Web of Science ID : WOS:000261285800007

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