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Chronobiology International
The Journal of Biological and Medical Rhythm Research
Volume 36, 2019 - Issue 6
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Original Articles

Impacts of high-sucrose diet on circadian rhythms in the small intestine of rats

, , , , , , & show all
Pages 826-837 | Received 24 Jan 2019, Accepted 05 Mar 2019, Published online: 28 Mar 2019
 

ABSTRACT

Excessive sucrose intake, known as fructose toxicity, leads to fatty liver, hyperlipidemia, and metabolic syndrome. Circadian disorders also contribute to metabolic syndrome. Here, we investigated the effect of excessive sucrose intake on circadian rhythms of the small intestine, the main location of sucrose absorption, to elucidate a mechanism of sucrose-induced abnormal lipid metabolism. Male Wistar rats were fed control starch or high-sucrose diets for 4 weeks. High-sucrose diet-induced fatty liver and hypertriglyceridemia in rats. Amplitudes of PER1/2 expression oscillations in the small intestine were reduced by excessive sucrose, while gene expression of GLUT5 and gluconeogenic enzymes was enhanced. These changes would contribute to interfering in lipid homeostasis as well as adaptive responses to control fructose toxicity in rats.

Acknowledgments

We thank the Japan Society for the Promotion of Science (JSPS) for funding supports (Recipient: H.O.; No.21658052; No.25292069; No.16H04922). And S.S. is a recipient of Otsuka Toshimi Scholarship Foundation.

Author contributions

S.S. and H.O. conceived and designed the experiments; S.S. and F.H. performed the experiments; S.S., F.H., M.U., Y.M., S.M. and S.I. analyzed data; N.N., S.I., S.M. and H.O. contributed reagents/materials/analysis tools; S.S. and H.O. wrote the manuscript.

Declaration of Interest statement

The authors declare no competing interests.

Data availability

The authors confirm that the data supporting the findings of this study are available within the article and its supplementary materials.

Supplementary Material

Supplemental data for this article can be accessed here.

Additional information

Funding

This work was supported by the Japan Society for the Promotion of Science [No.16H04922,No.21658052,No.25292069];

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