SatietyAssociatedwithCalorieRestrictionand Time-RestrictedFeeding:CentralNeuroendocrine Integration

Abstract

Thisreviewfocusesonsummarizingcurrentknowledgeonhowtime-restrictedfeeding(TRF)andcontinuouscaloricrestriction(CR)affectcentral neuroendocrine systems involved in regulating satiety. Several interconnected regions of the hypothalamus, brainstem, and cortical areas of the brain are involved in the regulation of satiety. Following CR and TRF, the increase in hunger and reduction in satiety signals of the melanocortin system [neuropeptide Y (NPY), proopiomelanocortin (POMC), and agouti-related peptide (AgRP)] appear similar between CR and TRF protocols, as do the dopaminergicresponses in the mesocorticolimbiccircuit.However, ghrelin and leptin signaling via the melanocortinsystem appears to improve energy balance signals and reduce hyperphagia following TRF, which has not been reported in CR. In addition to satiety systems, CR and TRF also influence circadian rhythms. CR influences the suprachiasmatic nucleus (SCN) or the primary circadian clock as seen by increased clock geneexpression.Incontrast,TRFappearstoaffectboththeSCNandtheperipheralclocks,asseenbyphasicchangesinthenon-SCN(potentiallythe elusivefoodentrainableoscillator)andmetabolicclocks.Theperipheralclocksareinfluencedbytheprimarycircadianclockbutarealsoentrainedby foodtiming,sleeptiming,andotherlifestyleparameters,whichcansupersedethemetabolicprocessesthatareregulatedbytheprimarycircadian clock. Taken together, TRF influences hunger/satiety, energy balance systems, and circadian rhythms, suggesting a role for adherence to CR in the long run if implemented using the TRF approach. However, these suggestions are based on only a few studies, and future investigations that use standardizedprotocolsfortheevaluationoftheeffectofthesedietpatterns(time,duration,mealcomposition,sufficientlypowered)arenecessary toverifythesepreliminaryobservations