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Chronic Effects of a High Sucrose Diet on Murine Gastrointestinal Nutrient Sensor Gene and Protein Expression Levels and Lipid Metabolism

Research output: Contribution to journalArticlepeer-review

Patrick O'Brien, Ge Han, Priya Ganpathy, Shweta Pitre, Yi Zhang, John Ryan, Pei Ying Sim, Scott V Harding, Robert Gray, Victor R Preedy, Thomas A B Sanders, Christopher P Corpe

Original languageEnglish
Article number137
Pages (from-to)1-26
Number of pages26
JournalInternational Journal of Molecular Sciences
Volume22
Issue number1
Early online date25 Dec 2020
DOIs
Accepted/In press16 Dec 2020
E-pub ahead of print25 Dec 2020
Published1 Jan 2021

Bibliographical note

Funding Information: Acknowledgments: This work was supported by the King’s College London studentship fund (P.O.). We are also grateful for the assistance of Arianna Psichas, Matt Arno and Estibaliz Aldecoa-Otalora for their gene micro array work. Publisher Copyright: © 2020 by the authors. Li-censee MDPI, Basel, Switzerland. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.

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Abstract

The gastrointestinal tract (GIT) plays a key role in regulating nutrient metabolism and appetite responses. This study aimed to identify changes in the GIT that are important in the development of diet related obesity and diabetes. GIT samples were obtained from C57BL/6J male mice chronically fed a control diet or a high sucrose diet (HSD) and analysed for changes in gene, protein and metabolite levels. In HSD mice, GIT expression levels of fat oxidation genes were reduced, and increased de novo lipogenesis was evident in ileum. Gene expression levels of the putative sugar sensor, slc5a4a and slc5a4b, and fat sensor, cd36, were downregulated in the small intestines of HSD mice. In HSD mice, there was also evidence of bacterial overgrowth and a lipopolysaccharide activated inflammatory pathway involving inducible nitric oxide synthase (iNOS). In Caco-2 cells, sucrose significantly increased the expression levels of the nos2, iNOS and nitric oxide (NO) gas levels. In conclusion, sucrose fed induced obesity/diabetes is associated with changes in GI macronutrient sensing, appetite regulation and nutrient metabolism and intestinal microflora. These may be important drivers, and thus therapeutic targets, of diet-related metabolic disease.

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