Next Article in Journal
Saccharin Increases Fasting Blood Glucose but Not Liver Insulin Resistance in Comparison to a High Fructose-Fed Rat Model
Previous Article in Journal
A Pecan-Rich Diet Improves Cardiometabolic Risk Factors in Overweight and Obese Adults: A Randomized Controlled Trial
Previous Article in Special Issue
Regulation of Muscle Glycogen Metabolism during Exercise: Implications for Endurance Performance and Training Adaptations
Article Menu
Issue 3 (March) cover image

Export Article

Open AccessArticle
Nutrients 2018, 10(3), 340; https://doi.org/10.3390/nu10030340

ChREBP-Knockout Mice Show Sucrose Intolerance and Fructose Malabsorption

1
Department of Diabetes and Endocrinology, Graduate School of Medicine, Gifu University, Gifu 501-1194, Japan
2
Gifu University Hospital Center for Nutritional Support and Infection Control, Gifu 501-1194, Japan
3
Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Gunma 371-8512, Japan
*
Author to whom correspondence should be addressed.
Received: 31 January 2018 / Revised: 7 March 2018 / Accepted: 7 March 2018 / Published: 12 March 2018
(This article belongs to the Special Issue Carbohydrate Metabolism in Health and Disease)
View Full-Text   |   Download PDF [4398 KB, uploaded 22 March 2018]   |  

Abstract

We have previously reported that 60% sucrose diet-fed ChREBP knockout mice (KO) showed body weight loss resulting in lethality. We aimed to elucidate whether sucrose and fructose metabolism are impaired in KO. Wild-type mice (WT) and KO were fed a diet containing 30% sucrose with/without 0.08% miglitol, an α-glucosidase inhibitor, and these effects on phenotypes were tested. Furthermore, we compared metabolic changes of oral and peritoneal fructose injection. A thirty percent sucrose diet feeding did not affect phenotypes in KO. However, miglitol induced lethality in 30% sucrose-fed KO. Thirty percent sucrose plus miglitol diet-fed KO showed increased cecal contents, increased fecal lactate contents, increased growth of lactobacillales and Bifidobacterium and decreased growth of clostridium cluster XIVa. ChREBP gene deletion suppressed the mRNA levels of sucrose and fructose related genes. Next, oral fructose injection did not affect plasma glucose levels and liver fructose contents; however, intestinal sucrose and fructose related mRNA levels were increased only in WT. In contrast, peritoneal fructose injection increased plasma glucose levels in both mice; however, the hepatic fructose content in KO was much higher owing to decreased hepatic Khk mRNA expression. Taken together, KO showed sucrose intolerance and fructose malabsorption owing to decreased gene expression. View Full-Text
Keywords: carbohydrate-responsive element-binding protein; ketohexokinase; fructose; glucose transporter 5; glucose transporter 2 carbohydrate-responsive element-binding protein; ketohexokinase; fructose; glucose transporter 5; glucose transporter 2
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Kato, T.; Iizuka, K.; Takao, K.; Horikawa, Y.; Kitamura, T.; Takeda, J. ChREBP-Knockout Mice Show Sucrose Intolerance and Fructose Malabsorption. Nutrients 2018, 10, 340.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Nutrients EISSN 2072-6643 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top