2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced change in intestinal function and pathology: Evidence for the involvement of arylhydrocarbon receptor-mediated alteration of glucose transportation

Takumi Ishida, Shoko Kan-O, Junpei Mutoh, Shuso Takeda, Yuji Ishii, Isamu Hashiguchi, Akifumi Akamine, Hideyuki Yamada

研究成果: ジャーナルへの寄稿記事

24 引用 (Scopus)

抄録

Although numerous studies have been performed to clarify the mechanism(s) underlying the toxicological responses induced by dioxins, their effect on the intestine is less well understood. To address this issue, we examined the effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the pathology and function of the intestine in arylhydrocarbon receptor (AhR)-sensitive (C57BL/6J) and -less-sensitive (DBA/2J) mice. A single oral administration of TCDD (100 μg/kg) to C57BL/6J mice produced changes in villous structure and nuclear/cytoplasm ratio in the epithelial cells of the intestine. Furthermore, in an oral glucose tolerance test, the serum glucose level was significantly increased in the C57BL/6J mouse but not in the DBA/2J mouse by TCDD treatment. In agreement with this, the expression of intestinal mRNAs coding sodium-glucose co-transporter 1 (SGLT1) and glucose transporter type 2 were increased only in C57BL/6J mice by TCDD. The increase in the former transporter was also confirmed from its protein level. The glucose level in the intestinal contents is thought to be one of the factors contributing to SGLT1 induction. Concerning with this, the intestinal activity of sucrase and lactase was significantly increased only in C57BL/6J mice by TCDD. These results suggest that while TCDD produces initial damage to the intestinal epithelium, the tissues induce SGLT1 to facilitate the absorption of glucose, which is expected, at least partially, to combat the wasting syndrome induced by TCDD. The data provided here also suggest that AhR is involved in the mechanism of SGLT1 induction.

元の言語英語
ページ(範囲)89-97
ページ数9
ジャーナルToxicology and Applied Pharmacology
205
発行部数1
DOI
出版物ステータス出版済み - 5 15 2005

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Pathology
Sodium-Glucose Transporter 1
Symporters
Glucose
Inbred C57BL Mouse
Intestines
Sodium
Inbred DBA Mouse
Glucose Transporter Type 2
Wasting Syndrome
Sucrase
Lactase
Gastrointestinal Contents
Dioxins
Intestinal Mucosa
Glucose Tolerance Test
Polychlorinated Dibenzodioxins
1,4-dioxin
Toxicology
Oral Administration

All Science Journal Classification (ASJC) codes

  • Toxicology
  • Pharmacology

これを引用

2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced change in intestinal function and pathology : Evidence for the involvement of arylhydrocarbon receptor-mediated alteration of glucose transportation. / Ishida, Takumi; Kan-O, Shoko; Mutoh, Junpei; Takeda, Shuso; Ishii, Yuji; Hashiguchi, Isamu; Akamine, Akifumi; Yamada, Hideyuki.

:: Toxicology and Applied Pharmacology, 巻 205, 番号 1, 15.05.2005, p. 89-97.

研究成果: ジャーナルへの寄稿記事

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abstract = "Although numerous studies have been performed to clarify the mechanism(s) underlying the toxicological responses induced by dioxins, their effect on the intestine is less well understood. To address this issue, we examined the effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the pathology and function of the intestine in arylhydrocarbon receptor (AhR)-sensitive (C57BL/6J) and -less-sensitive (DBA/2J) mice. A single oral administration of TCDD (100 μg/kg) to C57BL/6J mice produced changes in villous structure and nuclear/cytoplasm ratio in the epithelial cells of the intestine. Furthermore, in an oral glucose tolerance test, the serum glucose level was significantly increased in the C57BL/6J mouse but not in the DBA/2J mouse by TCDD treatment. In agreement with this, the expression of intestinal mRNAs coding sodium-glucose co-transporter 1 (SGLT1) and glucose transporter type 2 were increased only in C57BL/6J mice by TCDD. The increase in the former transporter was also confirmed from its protein level. The glucose level in the intestinal contents is thought to be one of the factors contributing to SGLT1 induction. Concerning with this, the intestinal activity of sucrase and lactase was significantly increased only in C57BL/6J mice by TCDD. These results suggest that while TCDD produces initial damage to the intestinal epithelium, the tissues induce SGLT1 to facilitate the absorption of glucose, which is expected, at least partially, to combat the wasting syndrome induced by TCDD. The data provided here also suggest that AhR is involved in the mechanism of SGLT1 induction.",
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AU - Ishida, Takumi

AU - Kan-O, Shoko

AU - Mutoh, Junpei

AU - Takeda, Shuso

AU - Ishii, Yuji

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AU - Akamine, Akifumi

AU - Yamada, Hideyuki

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