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Facilitatory effect of insulin treatment on hepatocellular carcinoma development in diabetes

https://tokushima-u.repo.nii.ac.jp/records/2007333
https://tokushima-u.repo.nii.ac.jp/records/2007333
6bfe8bba-effe-4364-80b3-440ef8e9bcab
名前 / ファイル ライセンス アクション
BMCRN_10_478.pdf BMCRN_10_478.pdf (1.71 MB)
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Item type 文献 / Documents(1)
公開日 2020-03-26
アクセス権
アクセス権 open access
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
出版社版DOI
関連識別子 https://doi.org/10.1186/s13104-017-2783-6
関連名称 10.1186/s13104-017-2783-6
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
タイトル
タイトル Facilitatory effect of insulin treatment on hepatocellular carcinoma development in diabetes
著者 ババ, ハヤト

× ババ, ハヤト

ja ババ, ハヤト

ja-Kana ババ, ハヤト

en Baba, Hayato

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クラノ, マコト

× クラノ, マコト

ja クラノ, マコト

ja-Kana クラノ, マコト

en Kurano, Makoto

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ニシダ, タケシ

× ニシダ, タケシ

ja ニシダ, タケシ

ja-Kana ニシダ, タケシ

en Nishida, Takeshi

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ハッタ, ヒデキ

× ハッタ, ヒデキ

ja ハッタ, ヒデキ

ja-Kana ハッタ, ヒデキ

en Hatta, Hideki

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ホカオ, リョウジ

× ホカオ, リョウジ

ja ホカオ, リョウジ

ja-Kana ホカオ, リョウジ

en Hokao, Ryoji

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常山, 幸一

× 常山, 幸一

WEKO 756
徳島大学 教育研究者総覧 289954/profile-ja.html
e-Rad 10293341

ja 常山, 幸一
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ja-Kana ツネヤマ, コウイチ

en Tsuneyama, Koichi

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抄録
内容記述 Background: To evaluate the effect of insulin treatment on the incidence and/or severity of hepatocellular carcinoma (HCC) in a mouse model of HCC based on diabetes.
Methods: We recently reported that neonatal streptozotocin (STZ) treatment causes type 1 diabetes and subsequent HCC in ddY, Institute for Animal Reproduction (DIAR) mice. Newborn male DIAR mice were divided into three groups based on STZ and insulin (INS) treatment. STZ was subcutaneously injected (60 mg/g) into the STZ-treated group (DIAR-nSTZ mice, N = 13) and the STZ/insulin-treated group (DIAR-nSTZ/INS mice, N = 20). A physiologic solution was injected into the control group (DIAR-control mice, N = 8) 1.5 days after birth. Insulin was subcutaneously injected into the DIAR-nSTZ/INS mice according to the following protocol: 2 IU/day at 4–5 weeks of age, 3 IU/day at 5–7 weeks of age, and 4 IU/day at 7–12 weeks of age. All mice were fed a normal diet and were subjected to physiological and histopathological assessments at 12 weeks of age.
Results: DIAR-nSTZ mice had significantly lower body weight and higher blood glucose levels than DIAR-control mice, whereas no significant differences were observed between DIAR-nSTZ/INS mice and control mice. At 12 weeks of age, lower weight of paratesticular fat and higher levels of total cholesterol, triglyceride, and free fatty acids were observed in DIAR-nSTZ mice compared to DIAR-control mice, whereas there were no significant differences between DIAR-nSTZ/INS mice and DIAR-control mice. In the livers of DIAR-nSTZ mice, HCC was observed in 15% of cases, and dysplastic nodules were observed in 77% of cases. In the livers of DIAR-nSTZ/INS mice, HCC was observed in 39% of cases and dysplastic nodules were observed in 61% of cases (p = 0.011). Moreover, the average tumor size was significantly larger in STZ/INS-treated mice than in STZ-treated mice. Immunohistochemical analysis demonstrated that the expression of ERK1/2, downstream substrates of insulin signaling that activate cell proliferation, was significantly higher in STZ/INS-treated mice compared to STZ-treated mice.
Conclusions: Insulin treatment promoted, rather than inhibited, the progression of liver carcinogenesis in DIAR-nSTZ mice. Hyperinsulinemia rather than hyperglycemia can accelerate the progression of HCC via insulin signaling.
キーワード
主題 Diabetes mellitus
キーワード
主題 Hepatocellular carcinoma
キーワード
主題 Insulin
キーワード
主題 Hyperinsulinemia
キーワード
主題 Hyperglycemia
書誌情報 en : BMC Research Notes

巻 10, p. 478, 発行日 2017-09-13
収録物ID
収録物識別子タイプ ISSN
収録物識別子 17560500
出版者
出版者 BioMed Central
出版者
出版者 Springer Nature
権利情報
権利情報 © The Author(s) 2017. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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識別子 333660
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言語 eng
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