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Role of Carbohydrate response element-binding protein in mediating dexamethasone-induced glucose transporter 5 expression in Caco-2BBE cells and during the developmental phase in mice

التفاصيل البيبلوغرافية
العنوان: Role of Carbohydrate response element-binding protein in mediating dexamethasone-induced glucose transporter 5 expression in Caco-2BBE cells and during the developmental phase in mice
المؤلفون: Soonjae Hwang, Sangbin Park, Jaewan Kim, Ah-Reum Oh, Ho-Jae Lee, Ji-Young Cha
المصدر: Animal Cells and Systems, Vol 28, Iss 1, Pp 15-24 (2024)
بيانات النشر: Taylor & Francis Group, 2024.
سنة النشر: 2024
المجموعة: LCC:Medicine (General)
LCC:Biology (General)
مصطلحات موضوعية: Fructose transporter, glucocorticoid hormone, dexamethasone, ChREBP, small intestine, Medicine (General), R5-920, Biology (General), QH301-705.5
الوصف: ABSTRACTGlucose transporter 5 (GLUT5), the main fructose transporter in mammals, is primarily responsible for absorbing dietary fructose in the small intestine. The expression of this intestinal gene significantly increases in response to developmental and dietary cues that reach the glucocorticoid receptor and carbohydrate response element-binding protein (ChREBP), respectively. Our study demonstrates that ChREBP is involved in the dexamethasone (Dex)-induced expression of GLUT5 in Caco-2BBE cells and the small intestine of both wild-type and ChREBP-knockout mice. Dex, a glucocorticoid, demonstrated an increase in GLUT5 mRNA levels in a dose- and time-dependent manner. While the overexpression of ChREBP moderately increased GLUT5 expression, its synergistic increase in the presence of Dex was noteworthy, whereas the suppression of ChREBP significantly reduced Dex-induced GLUT5 expression. Dex did not increase ChREBP protein levels but facilitated its nuclear translocation, thereby increasing the activity of the GLUT5 promoter. In vivo experiments conducted on 14-day-old mice pups treated with Dex for three days revealed that only wild-type mice (not ChREBP-knockout mice) exhibited Dex-mediated Glut5 gene induction, which further supports the role of ChREBP in regulating GLUT5 expression. Collectively, our results provide insights into the molecular mechanisms involved in the regulation of GLUT5 expression in response to developmental and dietary signals mediated by glucocorticoids and ChREBP.General significance: The transcription factor ChREBP is important for Dex-mediated Glut5 gene expression in the small intestine.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 19768354
2151-2485
1976-8354
Relation: https://doaj.org/toc/1976-8354; https://doaj.org/toc/2151-2485
DOI: 10.1080/19768354.2023.2301009
URL الوصول: https://doaj.org/article/c7122540d11f487bb98a9cdc28cb8c31
رقم الأكسشن: edsdoj.7122540d11f487bb98a9cdc28cb8c31
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:19768354
21512485
DOI:10.1080/19768354.2023.2301009