Enhanced Food-Anticipatory Circadian Rhythms in the Genetically Obese Zucker Rat

Mistlberger, Ralph E.; Marchant, Elliott G.

doi:10.1016/s0031-9384(98)00311-4

Cited by 70 publications

(55 citation statements)

References 51 publications

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“…Food was first restricted to ZT6 -ZT14 for 12 days, then animals were fed ad libitum for 3 days, and finally were food deprived for 24 h. Wheel-running data were collected by VitalView (MiniMitter) and were quantified by Actiview (MiniMitter) and Microsoft Excel. The ''anticipatory ratio'' and ''persistence ratio'' were calculated to quantify the differences in FAA between the mouse strain and its persistence under food deprivation (61). The anticipatory ratio was calculated as the ''anticipatory activity'' (mean number of wheel revolutions in the continuous bout of activity preceding food presentation at ZT6) divided by the mean number of wheel revolutions per day, averaged over the last 7 days of food restriction.…”

Section: Methodsmentioning

confidence: 99%

Stomach ghrelin-secreting cells as food-entrainable circadian clocks

LeSauter

Hoque

Weintraub

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

284

269

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Increases in arousal and activity in anticipation of a meal, termed “food anticipatory activity” (FAA), depend on circadian food-entrainable oscillators (FEOs), whose locations and output signals have long been sought. It is known that ghrelin is secreted in anticipation of a regularly scheduled mealtime. We show here that ghrelin administration increases locomotor activity in nondeprived animals in the absence of food. In mice lacking ghrelin receptors, FAA is significantly reduced. Impressively, the cumulative rise of activity before food presentation closely approximates a Gaussian function ( r = 0.99) for both wild-type and ghrelin receptor knockout animals, with the latter having a smaller amplitude. For both groups, once an animal begins its daily anticipatory bout, it keeps running until the usual time of food availability, indicating that ghrelin affects response threshold. Oxyntic cells coexpress ghrelin and the circadian clock proteins PER1 and PER2. The expression of PER1, PER2, and ghrelin is rhythmic in light–dark cycles and in constant darkness with ad libitum food and after 48 h of food deprivation. In behaviorally arrhythmic-clock mutant mice, unlike control animals, there is no evidence of a premeal decrease in oxyntic cell ghrelin. Rhythmic ghrelin and PER expression are synchronized to prior feeding, and not to photic schedules. We conclude that oxyntic gland cells of the stomach contain FEOs, which produce a timed ghrelin output signal that acts widely at both brain and peripheral sites. It is likely that other FEOs also produce humoral signals that modulate FAA.

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Section: Methodsmentioning

confidence: 99%

Stomach ghrelin-secreting cells as food-entrainable circadian clocks

LeSauter

Hoque

Weintraub

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

284

269

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“…Alternatively, because the insular cortex is known to be activated in response to anticipation of reward 30 and animal models of obesity show abnormally high food-anticipatory activity, [31][32][33] it is possible that exposure to the orosensory stimulation of a liquid meal elicited a more intense feeling of reward-anticipation in the obese and postobese than in the lean subjects. Both the increased craving and anticipation of reward may ultimately result in excessive energy intake.…”

Section: Discussionmentioning

confidence: 99%

Persistence of abnormal neural responses to a meal in postobese individuals

DelParigi¹,

Chen

Salbe³

et al. 2003

Int J Obes

167

131

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OBJECTIVE:To determine whether abnormal obese-like neural responses to a meal persist in postobese individuals, who achieved and maintained a normal body weight despite a past history of severe obesity. DESIGN AND SUBJECTS: Cross-sectional study of the brain's response to tasting and consuming a satiating meal in 11 postobese (age: 4076 y, body mass index (BMI): 23.671.9 kg/m 2 ), 23 obese (age: 2976 y, BMI: 39.673.8 kg/m 2 ) and 21 lean (age: 3379 y, BMI: 22.872.1 kg/m 2 ) subjects. MEASUREMENTS: Regional cerebral blood flow (rCBF, a marker of neural activity) at baseline (after a 36-h fast), after tasting and after consuming a satiating liquid meal was assessed using positron emission tomography and state-dependent changes (taste-baseline; satiation-baseline), and compared across groups. Subjective ratings of hunger and fullness were measured by a visual analogue scale and body fatness by dual-energy X-ray absorptiometry. RESULTS: In response to tasting the liquid meal, changes in rCBF were different in the obese as compared to the lean individuals (Po0.05, corrected for multiple comparisons) in the middle insula (peak voxel, x ¼ À41, y ¼ 1, z ¼ 8; Montreal Neurological Institute coordinates) and posterior cingulate cortex (peak voxel, x ¼ 17, y ¼ À47, z ¼ 40). The middle insular cortex exhibited a similar increase of neural activity in the obese and postobese subjects, whereas in the lean subjects the regional activity did not change. In the posterior cingulate cortex, the changes in rCBF in the postobese subjects were not different from those in the other groups. In response to a satiating amount of the same liquid meal, changes in rCBF were different in the obese as compared to the lean individuals (Po0.05, corrected for multiple comparisons) in the posterior hippocampus (peak voxel, x ¼ 21, y ¼ À45, x ¼ 4), posterior cingulate cortex (peak voxel, x ¼ 17, y ¼ À47, z ¼ 40), and amygdala (peak voxel, x ¼ 27, y ¼ 1, z ¼ À24). The posterior hippocampus exhibited a similar decrease of neural activity in the obese and postobese subjects, whereas in the lean subjects the regional activity increased. In the posterior cingulate cortex and amygdala, the changes in rCBF were not different between the postobese and lean individuals. None of the changes in neural activity were correlated with the age of the individuals, the subjective ratings of hunger and fullness, or the meal induced-changes in plasma glucose, insulin, or serum free fatty acids. CONCLUSION: Persistence of abnormal neural responses to a meal in the postobese individuals, a group at high risk for relapse, indicates that a predisposition to obesity may involve areas of the brain that control complex aspects of eating behavior including anticipation and reward, chemosensory perception, and autonomic control of digestion (insular cortex), as well as enteroception and learning/memory (hippocampus).

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“…Thus, the presentation of the 'anticipatory' or incentive stimuli effectively elicited behavioral changes provided that alternative learning (extinction) had not taken place. Parenthetically, in animals with a restricted daily feeding schedule, increased activity is apparent approximately 1-3 h prior to feeding ('feeding anticipatory activity') (Aragona et al, 2002;Mistlberger and Marchant, 1999;Ono et al, 1996), a behavior that is attenuated by treatment with a 5-HT receptor antagonist (Ono et al, 1996;Shibata et al, 1995;Persons et al, 1993). In the present investigation, the increased activity in the Cue Relevant rats was only evident upon presentation of the anticipatory cues, thus the behavioral and neurochemical changes likely reflected the effects of incentive salience rather than a time-dependent general arousal.…”

Section: Discussionmentioning

confidence: 99%

Anticipatory Cues Differentially Provoke In Vivo Peptidergic and Monoaminergic Release at the Medial Prefrontal Cortex

Merali

McIntosh

Anisman

2004

Neuropsychopharmacol

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Like primary reinforcers, the anticipation of reward ought to affect neurochemical release in brain regions, such as the medial prefrontal cortex (mPFC), which are associated with appraisal processes. To assess the neurochemical changes associated with anticipation, rats were exposed to the pairing of auditory (60-dB white noise), visual, and olfactory cues with the daily presentation of a palatable snack (Cue Relevant group). Rats of a second group were similarly trained, but for a 2-week period, the snack was no longer provided following cue presentation (Extinction group). In the third condition, the presentation of the snack and cues was uncorrelated (Cue Irrelevant group). Analyses of dialysates collected in vivo from the mPFC revealed that release of corticotropin-releasing hormone (CRH), gastrinreleasing peptide (GRP), and the 5-HT catabolite, 5-hydroxyindole acetic acid (5-HIAA), had increased bilaterally in response to the anticipatory cues, whereas DA release increased only within the right mPFC. In the case of CRH and GRP, these increases were also apparent in the extinction condition, despite the fact that behavioral arousal to the anticipatory cues (increased exploration, rearing, grooming, and vigilance) was only evident in the Cue Relevant condition. In contrast, the elevated DA and 5-HIAA were apparent exclusively in the Cue Relevant condition. Thus, CRH and GRP systems may serve to allocate salience and/or incentive reward value to biologically significant stimuli or reflect the emotional response to the anticipatory stimulus. The activity of DA and 5-HT neurons, in contrast, is more closely aligned with the cognitive appraisal of predictor stimuli.

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Enhanced Food-Anticipatory Circadian Rhythms in the Genetically Obese Zucker Rat

Cited by 70 publications

References 51 publications

Stomach ghrelin-secreting cells as food-entrainable circadian clocks

Stomach ghrelin-secreting cells as food-entrainable circadian clocks

Persistence of abnormal neural responses to a meal in postobese individuals

Anticipatory Cues Differentially Provoke In Vivo Peptidergic and Monoaminergic Release at the Medial Prefrontal Cortex

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