BMB Reports 2018; 51(9): 429-436  https://doi.org/10.5483/BMBRep.2018.51.9.197
Recent insights into the role of ChREBP in intestinal fructose absorption and metabolism
Ho-Jae Lee1 & Ji-Young Cha1,2,*
1Department of Biochemistry, Lee Gil Ya Cancer and Diabetes Institute, Gachon University College of Medicine, Incheon 21999, 2Gachon Medical Institute, Gil Medical Center, Incheon 21565, Korea
Correspondence to: Tel: +82-32-899-6070; Fax: +82-32-899-6032; E-mail: jycha1014@gachon.ac.kr
Received: July 27, 2018; Published online: September 30, 2018.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

cc This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Fructose in the form of sucrose and high fructose corn syrup is absorbed by the intestinal transporter and mainly metabolized in the small intestine. However, excess intake of fructose overwhelms the absorptive capacity of the small intestine, leading to fructose malabsorption. Carbohydrate response element-binding protein (ChREBP) is a basic helix-loop-helix leucine zipper transcription factor that plays a key role in glycolytic and lipogenic gene expression in response to carbohydrate consumption. While ChREBP was initially identified as a glucose-responsive factor in the liver, recent evidence suggests that ChREBP is essential for fructoseinduced lipogenesis and gluconeogenesis in the small intestine as well as in the liver. We recently identified that the loss of ChREBP leads to fructose intolerance via insufficient induction of genes involved in fructose transport and metabolism in the intestine. As fructose consumption is increasing and closely associated with metabolic and gastrointestinal diseases, a comprehensive understanding of cellular fructose sensing and metabolism via ChREBP may uncover new therapeutic opportunities. In this mini review, we briefly summarize recent progress in intestinal fructose metabolism, regulation and function of ChREBP by fructose, and delineate the potential mechanisms by which excessive fructose consumption may lead to irritable bowel syndrome.
Keywords: ChREBP, Fructose intolerance, Fructose metabolism, Irritable bowel syndrome, Small intestine
Figures
Fig. 1. Models for glucose and fructose transport across the intestinal epithelium. Glucose is transported into the enterocyte across the brush border membrane by the sodium glucose cotransporter 1 (SGLT1) and released across the basolateral membrane down the concentration gradients by glucose transporter 2 (GLUT2). The Na+/K+ pump in the basolateral membrane maintains the functional gradient of SGLT1. Fructose is transported through the brush border membrane and extruded basolaterally by facilitated diffusion via GLUT5.


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Funding Information
  • Ministry of Education, Science and Technology(Korean Ministry of Education, Science and Technology)
      10.13039/501100004085
     
  • National Research Foundation of Korea(NRF)
      10.13039/501100003725
      NRF-2016R1A2B4015866, NRF-2016R1D1A1B03935001

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