Neurological and stress related effects of shifting obese rats from a palatable diet to chow and lean rats from chow to a palatable diet. Physiol Behav

University of New South Wales, NSW 2052, Australia.
Physiology & Behavior (Impact Factor: 2.98). 11/2011; 105(4):1052-7. DOI: 10.1016/j.physbeh.2011.11.019
Source: PubMed


Rats exposed to an energy rich, cafeteria diet overeat and become obese. The present experiment examined the neural and behavioural effects of shifting obese rats from this diet to chow and lean rats from chow to the cafeteria diet. Two groups of male Sprague Dawley rats (n=24) were fed either highly palatable cafeteria diet or regular chow (30% vs. 12% energy as fat) for 16 weeks. Half of each group (n=12) was then switched to the opposing diet while the remainder continued on their original diet. The effects of diet switch on the response to restraint stress were assessed and rats were euthanised nine days after diet reversal. After 16 weeks of cafeteria diet, rats were 27% heavier than controls. Rats switched from chow to cafeteria diet (Ch-Caf) became hyperphagic and had increased dopamine D1, D2 and tyrosine hydroxylase mRNA expression in the ventral tegmental area (VTA) compared to rats switched from cafeteria to chow (Caf-Ch). Caf-Ch rats were hypophagic with significant reductions in white (16%) and brown (32%) adipose tissue mass, plasma leptin (34%) and fasting glucose (22%) compared to rats remaining on the cafeteria diet (Caf-Caf). Caf-Caf rats had an elevated plasma corticosterone response to restraint stress compared to Ch-Caf rats indicating that acute but not chronic consumption of palatable cafeteria diet may protect against stress. Caf-Ch rats had increased corticotropin releasing hormone mRNA expression in the dorsal hypothalamus compared to Ch-Ch rats implying that removal of the palatable diet activated the HPA axis. The results were discussed in terms of the links between palatability of diet, obesity and stress.

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    • "Indeed, while chow-only rats did not respond to footshock-induced reinstatement of food seeking, a pattern similar to previous findings [52], [53], the daily cafeteria group significantly increased lever pressing after 10 min of intermittent footshock. This heightened sensitivity to stress is consistent with studies in rodents showing that extended access to and withdrawal from palatable food causes adaptations in stress circuitry [22], [54]–[57]. In the present study, rats previously fed cafeteria diet, which restrict intake of chow once palatable food is no longer available, show greater sensitivity to stress-induced reinstatement, a finding that parallels the clinical observation that restraint eaters have a greater tendency to overeat when encountering a stressful situation [58], [59]. "
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    ABSTRACT: Background Relapse to unhealthy eating habits is a major problem in human dietary treatment. The individuals most commonly seeking dietary treatment are overweight or obese women, yet the commonly used rat reinstatement model to study relapse to palatable food seeking during dieting primarily uses normal-weight male rats. To increase the clinical relevance of the relapse to palatable food seeking model, here we pre-expose female rats to a calorically-dense cafeteria diet in the home-cage to make them overweight prior to examining the effect of this diet history on cue-, pellet-priming- and footshock-induced reinstatement of food seeking. Methods Post-natal day 32 female Long-Evans rats had seven weeks of home-cage access to either chow only or daily or intermittent cafeteria diet alongside chow. Next, they were trained to self-administer normally preferred 45 mg food pellets accompanied by a tone-light cue. After extinction, all rats were tested for reinstatement induced by discrete cue, pellet-priming, and intermittent footshock under extinction conditions. Results Access to daily cafeteria diet and to a lesser degree access to intermittent cafeteria diet decreased food pellet self-administration compared to chow-only. Prior history of these cafeteria diets also reduced extinction responding, cue- and pellet-priming-induced reinstatement. In contrast, modest stress-induced reinstatement was only observed in rats with a history of daily cafeteria diet. Conclusion A history of cafeteria diet does not increase the propensity for cue- and pellet-priming-induced relapse in the rat reinstatement model but does appear to make rats more susceptible to footshock stress-induced reinstatement.
    PLoS ONE 07/2014; 9(7):e102213. DOI:10.1371/journal.pone.0102213 · 3.23 Impact Factor
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    • "llection varied across experiments , with feeding time ranging from 12 to 24 weeks . The specifics of dietary duration for each experiment are outlined in Section 2 . 8 . Some animals received a dietary reversal procedure that transi - tioned animals from the HFD to a regular diet . For this , as the removal of palatable food is a known stressor ( South et al . , 2012 ) , animals were given a one - week period of mixed HFD and regular food to ease the stress of transition before complete rever - sal to the regular diet . All animals were weighed on date of arrival and re - weighed bi - weekly . 2 . 3 . Contextual pre - exposure fear conditioning paradigm A contextual pre - exposure fear - conditionin"
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    ABSTRACT: High-fat diet (HFD)-induced obesity is reaching worldwide proportions. In addition to causing obesity, HFDs also induce a variety of health disorders, which includes cognitive decline. Hippocampal function may be particularly vulnerable to the negative consequences of HFD, and it is suspected that 'primed' neuroinflammatory processes may mediate this response. To examine the link between diet, hippocampal function and neuroinflammation, male Wistar rats were fed a medium or HFD. Hippocampal memory function was measured using contextual pre-exposure fear conditioning (CPE-FC). Rats fed a HFD demonstrated impaired memory, an effect that was augmented with longer duration of HFD consumption. HFD-induced memory impairments were linked to potentiated levels of interleukin-1 beta (IL-1β) protein in the hippocampus 2 h after the foot-shock that occurs during CPE-FC. Central IL-1 receptor antagonism, with intracisterna magna (ICM) administration of hIL-1RA prior to the foot-shock prevented the diet-induced memory disruption, suggesting a critical role for IL-1β in this phenomenon. Additionally, obese animals whose diet regimen was reversed from HFD back to standard chow recovered memory function and did not demonstrate a foot-shock-induced hippocampal IL-1β increase. Interestingly, dietary reversal neutralized the negative impact of HFD on memory and IL-1β, yet animals maintained physiological evidence of obesity (increased body mass and serum leptin), indicating that dietary components, not body mass, may mediate the negative effects on memory.
    Brain Behavior and Immunity 07/2014; 42. DOI:10.1016/j.bbi.2014.06.017 · 5.89 Impact Factor
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    • "The second aim was to examine changes in feeding patterns among: (1) rats exposed to palatable foods for the first time; and (2) rats maintained on the cafeteria diet and then withdrawn from this diet for the first time (i.e., switched to standard lab chow only). Based on the results reported by South et al (2012), we expected that, relative to controls, rats exposed to palatable foods for the first time in the CLAMS would consume more, while rats withdrawn from the cafeteria diet for the first time in the CLAMS would consume less. "
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    ABSTRACT: Obesity is associated with excessive consumption of palatable, energy dense foods. The present study used an animal model to examine feeding patterns during exposure to and withdrawal from these foods. Male Sprague Dawley rats were exposed to standard lab chow only (Chow rats) or a range of cafeteria-style foods eaten by people (Caf rats). After 1, 4, 7 and 10 weeks of diet in their home cage, rats were subjected to 24-hour test sessions in a Comprehensive Lab Animal Monitoring System (CLAMS). In the first two test sessions, Chow rats were exposed to standard lab chow only while Caf rats were exposed to a biscuit and high-fat chow diet. In the final two test sessions, half the rats in each group were switched to the opposing diet. In each session we recorded numbers of bouts, energy consumed per bout, and intervals between bouts across the entire 24 hours. Relative to Chow rats, Caf rats initiated fewer bouts but consumed more energy per bout; however, their motivation to feed in the CLAMS declined over time, which was attributed to reduced variety of foods relative to their home cage diet. This decline in motivation was especially pronounced among Caf rats switched from the palatable CLAMS diet to standard lab chow only: the reduced energy intake in this group was due to a modest decline in bout frequency and a dramatic decline in bout size. Exposure to a cafeteria-diet, rich in variety, altered feeding patterns, reduced rats' motivation to consume palatable foods in the absence of variety, and further diminished motivation to feed when palatable foods were withdrawn and replaced with chow. Hence, variety is a key factor in driving excessive consumption of energy dense foods, and therefore, excessive weight gain.
    PLoS ONE 04/2014; 9(4):e93506. DOI:10.1371/journal.pone.0093506 · 3.23 Impact Factor
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