Early or delayed time-restricted feeding prevents metabolic impact of obesity in ice

Time-restricted feeding (TRF) initiated early during the dark phase prevents the metabolic consequences of a high-fat diet in rodent models. However, the metabolic consequences of delaying the initiation of TRF, akin to breakfast skipping in humans, is unclear. We assigned 8-week-old male C57BL/6J mice (n = 192) to chow or high-fat diet ad libitum (AL) for 4 weeks, before randomization to continue AL or 10 h of TRF, initiated at lights off (TRFe) or 4-h after lights off (TRFd) for a further 8 weeks. Oral glucose tolerance tests (1 g/kg), metabolic monitoring and body composition by echoMRl were performed, and tissues were collected at six time points. TRF reduced weight and fat mass vs AL, with a greater reduction in TRFe vs TRFd. TRF improved glucose tolerance and protected mice from high-fat diet-induced hepatosteatosis vs AL, with no difference between TRFe and TRFd. TRF increased the amplitude of Bmall, Cry1, Per2, Nampt, and Nocturnin mRNA levels in liver. A phase delay in Bmall, Cry1, Per2, Reverba, Nampt, NAD, Sirtl, and Nocturnin was observed in TRFd. Thus, delaying TRF limited the weight benefit and induced a phase delay in the hepatic clock, but improved metabolic health. Allowing more flexibility in when TRF is initiated may increase the translational potential of this dietary approach in humans.

Automated summary

Time-restricted feeding (TRF) implemented early during the dark phase can prevent metabolic consequences of a high-fat diet in rodents. Delaying the initiation of TRF may limit weight benefits and induce a phase delay in the hepatic clock, but improve metabolic health. Providing more flexibility in when TRF is initiated could increase its translational potential in humans.