Enhanced Urinary Bladder, Liver and Colon Carcinogenesis in Zucker Diabetic Fatty Rats in a Multiorgan Carcinogenesis Bioassay: Evidence for Mechanisms Involving Activation of PI3K Signaling and Impairment of P53 on Urinary Bladder Carcinogenesis
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- Ishii Naomi
- Department of Pathology, Osaka City University Graduate School of Medicine
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- Wei Min
- Department of Pathology, Osaka City University Graduate School of Medicine
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- Kakehashi Anna
- Department of Pathology, Osaka City University Graduate School of Medicine
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- Doi Kenichiro
- Department of Pathology, Osaka City University Graduate School of Medicine
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- Yamano Shotaro
- Department of Pathology, Osaka City University Graduate School of Medicine
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- Inaba Masaaki
- Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine
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- Wanibuchi Hideki
- Department of Pathology, Osaka City University Graduate School of Medicine
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In the present study, modifying effects of diabetes on carcinogenesis induced in type 2 diabetes mellitus model Zucker diabetic fatty (ZDF) rats were investigated using a multiorgan carcinogenesis bioassay. Our results demonstrated enhancement of urinary bladder, colon and liver carcinogenesis in ZDF rats treated with five types of carcinogens (DMBDD). Elevated insulin and leptin and decreased adiponectin levels in the serum may be responsible for the high susceptibility of type 2 diabetes mellitus model rats to carcinogenesis in these organs. Possible mechanisms of increased susceptibility of diabetic rats to bladder carcinogenesis could be activation of the PI3K pathway and suppression of p53 in the urothelium in consequence of the above serum protein alterations.
収録刊行物
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- Journal of Toxicologic Pathology
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Journal of Toxicologic Pathology 24 (1), 25-36, 2011
日本毒性病理学会
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詳細情報 詳細情報について
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- CRID
- 1390282679390865920
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- NII論文ID
- 130000675351
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- NII書誌ID
- AN10232280
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- ISSN
- 1881915X
- 09149198
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- NDL書誌ID
- 11076118
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可