Altered feeding differentially regulates circadian rhythms and energy metabolism in liver and muscle of rats

Abstract

Energy metabolism follows a diurnal pattern responding to the light/dark cycle and food availability. This study investigated the impact of restricting feeding to the daylight hours and feeding a high fat diet on circadian clock (bmal1, dbp, tef and e4bp4) and metabolic (pepck, fas, ucp3, pdk4) gene expression and markers of energy metabolism in muscle and liver of rats. The results show that in chow-fed rats switched to daylight feeding, the peak diurnal expression of genes in liver was shifted by 6-12h while expression of these genes in muscle remained in a similar phase to rats feeding ad libitum. High fat feeding during the daylight hours had limited effect on clock gene expression in liver or muscle but shifted the peak expression of metabolic genes (pepck, fas) in liver by 6-12h. The differential effects of daylight feeding on gene and protein expression in muscle and liver were accompanied by an 8% reduction in whole body energy expenditure, a 20-30% increased glycogen content during the light phase in muscle of day-fed rats and increased adipose tissue deposition per gram food consumed. These data demonstrate that a mismatch of feeding and light/dark cycle disrupts tissue metabolism in muscle with significant consequences for whole body energy homeostasis.

Decreased rates of operant food self-administration are associated with reward deficits in high-fat feeding mice

“…Indeed, we have observed that forced synchronization of food intake prevents obesity and allows recover reward performance [26,37,48]. Otherwise, mismatch between feeding and light/dark cycle has been shown to disrupt energy metabolism in skeletal muscle and has significant consequences for whole-body energy homeostasis [49].…”

Mouse strain-dependent variation in obesity and glucose homeostasis in response to high-fat feeding

“…Proteins were resolved by SDS-PAGE electrophoresis, and immunoblot analysis was conducted as described elsewhere [19,24,25]. Immunolabelled bands were quantified using ImageJ 1.44p software.…”

Interactions between endocrine and circadian systems

“…In a study on a mouse model of shift work, restoring normal food intake rhythms concurrently restores clock gene rhythmicity in the liver, as well as triglyceride, glycerol and GC rhythms, and gluconeogenesis (Barclay et al 2012). While these data suggest a direct link between peripheral clock regulation and energy homeostasis, the phase relationship between clock gene expression and the transcriptional activity of metabolismassociated genes is variable, suggesting an interplay between local and systemic factors (Reznick et al 2013). …”