Circadian disruption of feeding-fasting rhythm and its consequences for metabolic, immune, cancer, and cognitive processes.

Abstract

The circadian system is composed by a central hypothalamic clock at the suprachiasmatic nuclei (SCN) that communicates with peripheral circadian oscillators for daily coordination of behavior and physiology. The SCN entrain to the environmental 24-h light-dark (LD) cycle and drive daily rhythms of internal synchronizers such as core body temperature, hypothalamic-hypophysary hormones, sympathetic/parasympathetic activity, as well as behavioral and feeding-fasting rhythms, which supply signals setting core molecular clocks at central and peripheral tissues. Steady phase relationships between the SCN and peripheral oscillators keep homeostatic processes such as microbiota/microbiome composition/activity, metabolic supply/demand, energy balance, immunoinflammatory process, sleep amount and quality, psychophysiological stress, etc. Indeed, the risk of health alterations increase when these phase relationships are chronically changed prompting circadian disruption (CD), as occurring after sudden LD cycle changes (so-called jet-lag), or due to changes of activity/feeding-rest/fasting rhythm with respect to LD cycles (as humans subjected to nightwork, or restricting food access at rest in mice). Typical pathologies observed in animal models of CD and epidemiological studies include metabolic syndrome, type-2 diabetes, obesity, chronic inflammation, cancer, sleep disruption, decrease in physical and cognitive performance, and mood, among others. The present review discusses different aspects of such physiological dysregulations observed in animal models of CD having altered feeding-fasting rhythms, with potential translation to human health.