Withdrawal from free-choice high-fat high-sugar diet induces craving only in obesity-prone animals

Department of Neuroscience Functional Pharmacology, Uppsala University, Uppsala, Sweden.
Psychopharmacology (Impact Factor: 3.88). 03/2009; 204(3):431-43. DOI: 10.1007/s00213-009-1474-y
Source: PubMed


Vulnerability for weight gain is an individual trait. Obese people undertake dieting, but permanent weight loss is difficult to attain due to repeated phases of relapse to excess consumption.
In this study, male Wistar rats were trained to operantly self-administer pellets followed by free-choice access in the homecage to high-fat high-sugar (HFHS) diet consisting of 30% sucrose, lard, standard rodent chow and water. Animals were divided into obesity-prone (OP) and obesity-resistant (OR) groups based on relative weight gain compared to normally fed controls despite equal consumption of HFHS.
After 4 weeks of HFHS access, OP and OR animals did not differ in motivation for food pellets in terms of progressive ratio break point, lever pressing or response rate. However, upon discontinuation of the HFHS diet, differences between the OP and OR groups were noted. OP animals increased their motivation (i.e. craving) during the second withdrawal week and reduced time spent in the centre of an open field (increased anxiety) compared to the OR animals. Both OP and OR animals consumed less of the standard rodent chow during the first week of withdrawal when compared to normally fed controls. But, while the OR animals quickly returned to control levels of food consumption, OP animals continued to consume less standard rodent chow.
The results show for the first time that withdrawal from free-choice HFHS induces craving that is specific to the OP animals and suggests that OP individuals may have withdrawal symptoms that are similar to those induced by addictive drugs.

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    • "These reward pathways are highly conserved across species and have been associated with altered responsiveness to reward (e.g., food) in obesity. Studies have demonstrated diminished responsiveness to perform food motivated behaviors and rewarding intracranial self-stimulation in obese rats (Volkow and Wise, 2005; la Fleur et al., 2007; Pickering et al., 2009; Johnson and Kenny, 2010) and reduced sensitivity to reward (measured by ratings of motivation and pleasure derived from engaging in rewarding behaviors) in obese humans (Davis et al., 2004). "
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    ABSTRACT: A range of animal and human data demonstrates that excessive consumption of palatable food leads to neuroadaptive responses in brain circuits underlying reward. Unrestrained consumption of palatable food has been shown to increase the reinforcing value of food and weaken inhibitory control; however, whether it impacts upon the sensory representations of palatable solutions has not been formally tested. These experiments sought to determine whether exposure to a cafeteria diet consisting of palatable high fat foods impacts upon the ability of rats to learn about food-associated cues and the sensory properties of ingested foods. We found that rats fed a cafeteria diet for 2 weeks were impaired in the control of Pavlovian responding in accordance to the incentive value of palatable outcomes associated with auditory cues following devaluation by sensory-specific satiety. Sensory-specific satiety is one mechanism by which a diet containing different foods increases ingestion relative to one lacking variety. Hence, choosing to consume greater quantities of a range of foods may contribute to the current prevalence of obesity. We observed that rats fed a cafeteria diet for 2 weeks showed impaired sensory-specific satiety following consumption of a high calorie solution. The deficit in expression of sensory-specific satiety was also present 1 week following the withdrawal of cafeteria foods. Thus, exposure to obesogenic diets may impact upon neurocircuitry involved in motivated control of behavior.
    Frontiers in Psychology 08/2014; 5:852. DOI:10.3389/fpsyg.2014.00852 · 2.80 Impact Factor
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    • "The animals withdrawn from the CAF diet behaved like CAF-fed animals in most of the behavioural tests except in the open field, where they showed a decrease in the time spent in the centre, thereby indicating increased anxiety compared to the CAF-fed animals. This is consistent with an interesting study of Pickering et al [53] who also found increased anxiety in the open field in diet-induced obese rats after 2 weeks of diet withdrawal. Animals receiving a high-fat high-sugar (HFHS) diet for 7 weeks were divided into obesity-prone and obesity-resistant groups based on the relative weight gain and tested 2 weeks after withdrawal. "
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    ABSTRACT: Among adolescents, overweight, obesity and metabolic syndrome are rapidly increasing in recent years as a consequence of unhealthy palatable diets. Animal models of diet-induced obesity have been developed, but little is known about the behavioural patterns produced by the consumption of such diets. The aim of the present study was to determine the behavioural and biochemical effects of a cafeteria diet fed to juvenile male and female rats, as well as to evaluate the possible recovery from these effects by administering standard feeding during the last week of the study. Two groups of male and female rats were fed with either a standard chow diet (ST) or a cafeteria (CAF) diet from weaning and for 8 weeks. A third group of males (CAF withdrawal) was fed with the CAF diet for 7 weeks and the ST in the 8th week. Both males and females developed metabolic syndrome as a consequence of the CAF feeding, showing overweight, higher adiposity and liver weight, increased plasma levels of glucose, insulin and triglycerides, as well as insulin resistance, in comparison with their respective controls. The CAF diet reduced motor activity in all behavioural tests, enhanced exploration, reduced anxiety-like behaviour and increased social interaction; this last effect was more pronounced in females than in males. When compared to animals only fed with a CAF diet, CAF withdrawal increased anxiety in the open field, slightly decreased body weight, and completely recovered the liver weight, insulin sensitivity and the standard levels of glucose, insulin and triglycerides in plasma. In conclusion, a CAF diet fed to young animals for 8 weeks induced obesity and metabolic syndrome, and produced robust behavioural changes in young adult rats, whereas CAF withdrawal in the last week modestly increased anxiety, reversed the metabolic alterations and partially reduced overweight.
    PLoS ONE 01/2014; 9(1):e85049. DOI:10.1371/journal.pone.0085049 · 3.23 Impact Factor
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    • "The powerful rewarding properties of food have been paralleled to those of drugs of abuse, and thus overeating has been compared to addiction (Dagher, 2009; Avena and Gold, 2011). Removal of a palatable diet can induce withdrawal-like behaviors (Cottone et al., 2009) and can cause rodents to endure aversive stimuli in order to regain access to palatable food (Pickering et al., 2009). "
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    ABSTRACT: The current obesity "epidemic" in the developed world is a major health concern; over half of adult Canadians are now classified as overweight or obese. Although the reasons for high obesity rates remain unknown, an important factor appears to be the role stressors play in overconsumption of food and weight gain. In this context, increased stressor exposure and/or perceived stress may influence eating behavior and food choices. Stress-induced anorexia is often noted in rats exposed to chronic stress (e.g., repeated restraint) and access to standard Chow diet; associated reduced consumption and weight loss. However, if a similar stressor exposure takes place in the presence of palatable, calorie dense food, rats often consume an increase proportion of palatable food relative to Chow, leading to weight gain and obesity. In humans, a similar desire to eat palatable or "comfort" foods has been noted under stressful situations; it is thought that this response may potentially be attributable to stress-buffering properties and/or through activation of reward pathways. The complex interplay between stress-induced anorexia and stress-induced obesity is discussed in terms of the overlapping circuitry and neurochemicals that mediate feeding, stress and reward pathways. In particular, this paper draws attention to the bombesin family of peptides (BBs) initially shown to regulate food intake and subsequently shown to mediate stress response as well. Evidence is presented to support the hypothesis that BBs may be involved in stress-induced anorexia under certain conditions, but that the same peptides could also be involved in stress-induced obesity. This hypothesis is based on the unique distribution of BBs in key cortico-limbic brain regions involved in food regulation, reward, incentive salience and motivationally driven behavior.
    Frontiers in Neuroscience 10/2013; 7(7):193. DOI:10.3389/fnins.2013.00193 · 3.66 Impact Factor
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