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

Pickering, Chris; Alsiö, Johan; Hulting, Anna‐Lena; Schiöth, Helgi B.

doi:10.1007/s00213-009-1474-y

Cited by 81 publications

(68 citation statements)

References 47 publications

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“…High-fat food withdrawal and reward S Sharma et al that contribute to food cravings following HFD withdrawal, 20 removal of high-fat food following long-term intake is sufficient to enhance motivation and cravings for palatable foods. In addition to increasing motivation for palatable food, HFD removal potentiated anxiety-like behaviour.…”

Section: Discussionmentioning

confidence: 99%

“…Cottone et al [16][17][18] found that withdrawal from extended, intermittent access to palatable food increases anxiety and decreases effortbased responding for less palatable chow, an effect linked to elevated corticotrophin-releasing factor receptor-1 (CRF-R1) signalling in the amygdala. 19 HFD removal is reported to increase operant responding for sucrose rewards in obesity-prone but not obesity-resistant rats, 20 however, it is not known if withdrawal from chronic high-fat feeding increases anxiety and palatable food reward, independent of genetic factors that enhance susceptibility to weight gain and which neurobiological changes are involved.…”

Section: Introductionmentioning

confidence: 98%

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Adaptations in brain reward circuitry underlie palatable food cravings and anxiety induced by high-fat diet withdrawal

2012

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OBJECTIVE:To identify the emotional and motivational processes that reinstate palatable food intake following removal of high-fat diet (HFD) and associated neuroadaptations tied to neurochemical and behavioural changes underlying dopaminergic function. METHODS: Adult male C57Bl6 mice were placed on a HFD (58% kcal fat) or ingredient-matched, low-fat diet (LFD; 11% kcal fat) for 6 weeks. At the end of diet-regimen mice were either maintained on their respective diets, or HFD and LFD were replaced with normal chow (withdrawal). Effort-based operant responding for sucrose and high-fat food rewards was measured along with basal and stress-induced corticosterone levels and anxiety (elevated-plus maze). Protein levels for tyrosine hydroxylase (TH), corticosterone releasing factor type 1 receptor (CRF-R1), brain-derived neurotrophic factor (BDNF), phospho-CREB (pCREB) and DFosB (truncated splice variant of FosB) were assessed in the amygdala, nucleus accumbens (NAc) and ventral tegmental area (VTA) via western immunoblotting. RESULTS: Six weeks of HFD resulting in significant weight gain elicited sucrose anhedonia, anxiety-like behaviour and hypothalamic-pituitary-adrenocortical axis (HPA) hypersensitivity to stress. Withdrawal from HFD but not LFD-potentiated anxiety and basal corticosterone levels and enhanced motivation for sucrose and high-fat food rewards. Chronic high-fat feeding reduced CRF-R1 and increased BDNF and pCREB protein levels in the amygdala and reduced TH and increased DFosB protein in NAc and VTA. Heightened palatable food reward in mice withdrawn from HFD coincided with increased BDNF protein levels in NAc and decreased TH and pCREB expression in the amygdala. CONCLUSION: Anhedonia, anxiety and sensitivity to stressors develops during the course of HFD and may have a key role in a vicious cycle that perpetuates high-fat feeding and the development of obesity. Removal of HFD enhances stress responses and heightens vulnerability for palatable foods by increasing food-motivated behaviour. Lasting changes in dopamine and plasticityrelated signals in reward circuitry may promote negative emotional states, overeating and palatable food relapse.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Adaptations in brain reward circuitry underlie palatable food cravings and anxiety induced by high-fat diet withdrawal

2012

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“…Additionally, OP animals have gained more weight than the OR and control group, even though there were no significant differences in food intake between the experimental groups. It is also noteworthy that total amount of consumed calories did not correlate with body weight increase [82].…”

Section: Pre-clinical Models Of Binge Eatingmentioning

confidence: 98%

Binge eating in pre-clinical models

Rospond

Szpigiel

Sadakierska‐Chudy

et al. 2015

Pharmacological Reports

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Obesity is a globally widespread disease. Approximately 35% of world population has the problem of inappropriate body weight due to sedentary lifestyle, excessive food consumption and the lack of physical activity. In the course of many years, several pharmacological anti-obesity drugs have been discovered. Most of them, however, possess severe side effects. Recent findings suggest that disturbed functioning of the reward system can be involved in the development of obesity. The data coming from clinical and animal studies provide new evidence that links excessive food consumption with compulsive behavior that can lead to binge eating disease occurrence. In this review we discuss most commonly used animal models of binge eating such as restriction/refeeding, limited access and stress schedule model, and related to them neurobiological findings as well. We also present new, anti-obesity drugs, which are characterized by central mechanism of action.

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“…It has been hypothesized that individuals expressing the Taq1 A1 allele are more susceptible to seek and consume palatable food as a form of compensatory behaviour [71]. Individual vulnerabilities have also been observed in rodents: the motivation to consume palatable food is more pronounced in obesity-prone rats [73], and rats more sensitive to the incentive properties of palatable food are significantly more sensitive to the reinforcing effect of cocaine [74].…”

Section: Food Addiction: Classic Substance Dependence?mentioning

confidence: 99%

Neuroscience of Reward: Implications for Food Addiction and Nutrition Policy

Horman¹,

Leri²

2016

J Nutr Food Sci

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According to the World Health Organization, unhealthy diet is one key contributor to the development of noncommunicable diseases. The global response to this problem has primarily involved the implementation of nutritional policies intended on raising public awareness, and providing information through nutritional guidelines and product labels. However, there is experimental evidence suggesting that certain foods may promote addictive processes and consequent unhealthy dietary choices. This review discusses neurobiological mechanisms of reward involved in the consumption of refined sugars and fats, and the aforementioned indicators of their addictive characteristics. By acknowledging that these foods can act on brain reward systems to promote excessive or addictive consumption, policy makers may need to address issues of unhealthy diets by considering approaches that target availability, regulations within the food industry, taxation and advertising.

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

Abstract: 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.

Cited by 81 publications

References 47 publications

Adaptations in brain reward circuitry underlie palatable food cravings and anxiety induced by high-fat diet withdrawal

Adaptations in brain reward circuitry underlie palatable food cravings and anxiety induced by high-fat diet withdrawal

Binge eating in pre-clinical models

Neuroscience of Reward: Implications for Food Addiction and Nutrition Policy

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