Circadian clocks enable the anticipation of daily events, conferring a considerable advantage for saving time and the efficient use of energy. The central clock activates the sympathetic nervous system and increases body temperature and blood pressure ahead of the active phase, facilitating the start of activities. Digestion/absorption systems also prepare before breakfast based on the time of local clocks [7•, 10]. Because colonic motility also is regulated by the local clocks, gastrointestinal symptoms are prevalent among shift workers and time-zone travelers [11]. In addition to local physiological events in tissues, some activity rhythms also are affected by feeding. Scheduled feeding elicits food anticipatory activity that is independent of light/dark cues and is perceived as food-seeking behavior approximately 2 hours before feeding [7•, 12]. This activity rhythm persists in rodents with SCN lesions, indicating that the central clock is not essential for food anticipatory activity. Because food available timing can be occasionally restricted in the wild, circadian anticipatory control of behavior and energy metabolism probably increases food usage and energy efficiency. Indeed, many studies have shown that circadian clocks intimately control energy metabolism [13]. Many genes associated with glucose and lipid homeostasis, especially those encoding rate limiting enzymes in various metabolic processes, are under circadian control. Thus, mutations or deletions of clock genes lead to metabolic disorders [14]. Mice with mutant Clock have attenuated feeding rhythm, hyperphagic, and obesity as well as altered gluconeogenesis, insulin insensitivities, and lipid homeostasis [15, 16]. Glucose and lipid homeostasis are similarly impaired in Bmal1 knockout mice [17, 18], and altered lipid metabolism, attenuated nocturnal food intake with total overeating, and developing significant obesity on high-fat diet are reported in Per2 knockout mice [19, 20]. A few studies have suggested an association between genetic variance in clock genes and metabolic risk in humans [14, 21•]. In addition, an epigenetic state of clock genes might be associated with obesity [22]. These genetic associations indicate mutual interaction among circadian clocks, metabolism, and nutrition.
Nutrients, Clock Genes, and Chrononutrition
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