Abstract

The etiology of metabolic syndrome involves several complicated factors. One of the main factors contributing to metabolic syndrome has been proposed to be excessive intake of sucrose, which disturbs hepatic lipid metabolism, resulting in fatty liver. However, the mechanism by which sucrose induces fatty liver remains to be elucidated. Considering feeding behavior important for metabolism, we investigated whether time-restricted feeding of high sucrose diet (HSD), only in the active phase (the dark phase of the daily light/dark cycle), would ameliorate adverse effects of sucrose on lipid homeostasis in rats. Male Wistar rats, fed either an ad libitum (ad lib.) or time-restricted control starch diet (CD) or HSD were investigated. Rats fed ad lib. (CD and HSD) completed approximately 20% of food intake in the daytime. Time-restricted feeding did not significantly suppress total food intake of rats. However, time-restricted feeding of HSD significantly suppressed the increased plasma triglyceride levels. Moreover, time-restricted feeding also ameliorated HSD-induced liver lipid accumulation, whereas circadian oscillations of liver clock gene or transcriptional factor gene expression for lipid metabolism were not altered significantly. These results demonstrated that restricting sucrose intake only during the active phase in rats ameliorates the abnormal lipid metabolism caused by excess sucrose intake.

Highlights

  • Metabolic syndrome is a cluster of symptoms, including type 2 diabetes, hypertension, hyperlipidemia, and central obesity, without internationally agreed definition[1]

  • Body weight gain had no obvious change among CDA, HSDA, and HSDR groups, while group CDR showed lowered body weight gain (Table 2)

  • Our results demonstrated that time-restricted feeding of high sucrose diet (HSD) attenuated both blood and hepatic lipid accumulation, resulting from excess sucrose intake

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Summary

Introduction

Metabolic syndrome is a cluster of symptoms, including type 2 diabetes, hypertension, hyperlipidemia, and central obesity, without internationally agreed definition[1]. Nowadays it is a global problem threatening human health. A monosaccharide of sucrose hydrolysis, was concluded to play an important role in the pathogenesis of metabolic diseases, including non-alcoholic fatty liver and hyperlipidemia [4,5]. We found that time-restricted feeding of HSD suppressed the excess sucrose-induced lipid accumulation effectively both in blood and liver, when compared with rats fed HSD ad lib., without significantly altering the circadian oscillations of clock gene expression in liver

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