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With chronotherapy, drug administration is synchronized with daily rhythms in drug clearance and pharmacokinetics. Daily rhythms in gene expression are centrally mastered by the suprachiasmatic nucleus of the hypothalamus as well as by tissue clocks containing similar molecular mechanisms in peripheral organs. The central timing system is sensitive to changes in the external environment such as those of the light-dark cycle, meal timing and meal composition. We investigated how changes in diet composition and meal timing would affect the daily hepatic expression rhythms of the nuclear receptors PXR and CAR and of enzymes involved in P450 mediated drug metabolism, as such changes could have consequences for the practice of chronotherapy.    Materials and methods  Rats were subjected to either a regular chow or a free choice high-fat-high-sugar (fcHFHS) diet. These diets were provided  ad libitum , or restricted to either the light phase or the dark phase. In a second experiment, rats had access to chow either  ad libitum  or in 6 meals equally distributed over 24 hours.    Results   Pxr ,  Alas1  and  Por  displayed significant day-night rhythms under  ad libitum  chow fed conditions, which for  Pxr  was disrupted under fcHFHS diet conditions. Although no daily rhythms were detected in expression of  CAR ,  Cyp2b2  and  Cyp3a2 , the fcHFHS diet did affect basal expression of these genes. In chow fed rats, dark phase feeding induced a diurnal rhythm in  Cyp2b2  expression while light phase feeding induced a diurnal rhythm in  Car  expression and completely shifted the peak expression of  Pxr ,  Car ,  Cyp2b2 ,  Alas1  and  Por . The 6-meals-a-day feeding only abolished the  Pxr  rhythm but not the rhythms of the other genes.    Conclusion  We conclude that although nuclear receptors and enzymes involved in the regulation of hepatic drug metabolism are sensitive to meal composition, changes in meal timing are mainly effectuated via changes in the molecular clock.

Effects of meal composition and meal timing on the expression of genes involved in hepatic drug metabolism in rats