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      Large, binge-type meals of high fat diet change feeding behaviour and entrain food anticipatory activity in mice *

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          Highlights

          • Rapid adaptation of feeding behaviour to scheduled palatable diet access

          • No evidence of reduced feeding (hypophagia) prior to scheduled palatable meals

          • Mice exhibit food anticipatory activity (FAA) prior to scheduled palatable meals

          • Continuing presence of FAA when scheduled palatable mealsare withdrawn

          • Immediate hyperphagic response once the palatable meals are restored after 7 days

          Abstract

          Male C57BL/6 mice fed ad libitum on control diet but allowed access to a palatable high fat diet (HFD) for 2 h a day during the mid-dark phase rapidly adapt their feeding behaviour and can consume nearly 80% of their daily caloric intake during this 2 h-scheduled feed. We assessed food intake microstructure and meal pattern, and locomotor activity and rearing as markers of food anticipatory activity (FAA). Schedule fed mice reduced their caloric intake from control diet during the first hours of the dark phase but not during the 3-h period immediately preceding the scheduled feed. Large meal/binge-like eating behaviour during the 2-h scheduled feed was characterised by increases in both meal number and meal size. Rearing was increased during the 2-h period running up to scheduled feeding while locomotor activity started to increase 1 h before, indicating that schedule-fed mice display FAA. Meal number and physical activity changes were sustained when HFD was withheld during the anticipated scheduled feeding period, and mice immediately binged when HFD was represented after a week of this “withdrawal” period. These findings provide important context to our previous studies suggesting that energy balance systems in the hypothalamus are not responsible for driving these large, binge-type meals. Evidence of FAA in HFD dark phase schedule-fed mice implicates anticipatory processes in binge eating that do not involve immediately preceding hypophagia or regulatory homeostatic signalling.

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          Most cited references42

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          Circadian timing of food intake contributes to weight gain.

          Studies of body weight regulation have focused almost entirely on caloric intake and energy expenditure. However, a number of recent studies in animals linking energy regulation and the circadian clock at the molecular, physiological, and behavioral levels raise the possibility that the timing of food intake itself may play a significant role in weight gain. The present study focused on the role of the circadian phase of food consumption in weight gain. We provide evidence that nocturnal mice fed a high-fat diet only during the 12-h light phase gain significantly more weight than mice fed only during the 12-h dark phase. A better understanding of the role of the circadian system for weight gain could have important implications for developing new therapeutic strategies for combating the obesity epidemic facing the human population today.
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            Circadian food-anticipatory activity: formal models and physiological mechanisms.

            Rats and other species exhibit food-anticipatory activity (FAA) to daily mealtime under circadian (24 h) food access schedules. A critical review of several explanatory models indicates that hourglass clocks and associative learning processes are inadequate to explain many properties of FAA in intact and suprachiasmatic nuclei ablated rodents. A computational learning model, involving circadian clock consultation and phase memory, accounts for some but not all of these properties. An entrainment model, invoking separate, compound food- and light-entrainable oscillators, provides a more complete account of FAA. However, FAA may be simulated best by a model that combines oscillator entrainment with clock consultation and memory for circadian phase. Species as diverse as bees, birds, and mammals appear to share many features of FAA in common; differences may be explained in terms of oscillator organization and the ability to represent multiple circadian phases memorially. Physiological mechanisms of FAA are largely unknown; strategies for localization of entrainment pathways and oscillators, and a modest data base, are reviewed.
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              Circadian Desynchrony Promotes Metabolic Disruption in a Mouse Model of Shiftwork

              Shiftwork is associated with adverse metabolic pathophysiology, and the rising incidence of shiftwork in modern societies is thought to contribute to the worldwide increase in obesity and metabolic syndrome. The underlying mechanisms are largely unknown, but may involve direct physiological effects of nocturnal light exposure, or indirect consequences of perturbed endogenous circadian clocks. This study employs a two-week paradigm in mice to model the early molecular and physiological effects of shiftwork. Two weeks of timed sleep restriction has moderate effects on diurnal activity patterns, feeding behavior, and clock gene regulation in the circadian pacemaker of the suprachiasmatic nucleus. In contrast, microarray analyses reveal global disruption of diurnal liver transcriptome rhythms, enriched for pathways involved in glucose and lipid metabolism and correlating with first indications of altered metabolism. Although altered food timing itself is not sufficient to provoke these effects, stabilizing peripheral clocks by timed food access can restore molecular rhythms and metabolic function under sleep restriction conditions. This study suggests that peripheral circadian desynchrony marks an early event in the metabolic disruption associated with chronic shiftwork. Thus, strengthening the peripheral circadian system by minimizing food intake during night shifts may counteract the adverse physiological consequences frequently observed in human shift workers.
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                Author and article information

                Contributors
                Journal
                Appetite
                Appetite
                Appetite
                Academic Press
                0195-6663
                1095-8304
                01 June 2014
                01 June 2014
                : 77
                : 100
                : 62-73
                Affiliations
                [a ]University of Aberdeen, Rowett Institute of Nutrition and Health, Ingestive Behaviour Group, Bucksburn, Aberdeen, UK
                [b ]AstraZeneca, Mereside, Alderley Park, Macclesfield, UK
                Author notes
                [* ]Corresponding author. j.mercer@ 123456abdn.ac.uk
                [1]

                Present addresses: Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, SE-405 30 Gothenburg, Sweden

                [2]

                Present addresses: School of Pharmacy, Keele University, Staffordshire ST5 5BG, UK.

                Article
                S0195-6663(14)00114-7
                10.1016/j.appet.2014.02.020
                4152876
                24631639
                81dcfceb-ae0f-456b-9935-f99345d552ef
                © 2014 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

                History
                : 30 August 2013
                : 26 February 2014
                : 28 February 2014
                Categories
                Research Report

                feeding pattern,palatability,food anticipation,scheduled feeding,binge-like eating,mouse

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