Sucrose consumption can cause obesity and nonalcoholic fatty liver disease (NAFLD). NAFLD is associated with the disruption of circadian rhythms. We compared the alterations in NAFLD circadian rhythms induced by a high-sucrose diet (HSD) with those induced by a high-fat diet (HFD) in mice. After 8 weeks of feeding, the liver triglyceride level was increased by HSD feeding and by HFD feeding. In the liver of HSD-fed mice, the amplitude of Rorγ and the mesor (time series 24 h mean value based on the distribution of values across the cycle of the circadian rhythm) of Rorγ and Per2 were increased in comparison to those of control-diet fed mice. Compared with the HFD-fed mice, the HSD-fed mice showed increased circadian amplitude of variation in Rorγ, Per2, Cry1, and Cry2 and mesors of Rorγ, Per2, and Cry1 in the liver. Rorγ appeared to play critical roles in the entrainment of HSD into the liver circadian system, and the increased expressions of Crys and Per2 might disrupt circadian rhythms. Thus, disruption of circadian rhythms by HSD and HFD may accelerate the accumulation of liver lipid through different mechanisms.
Keywords: High-sucrose diet; circadian rhythms; clock genes; clock-controlled nuclear receptor; high-fat diet; nonalcoholic fatty liver disease.