A high‐fat diet prevents and reverses the development of activity‐based anorexia in rats

Brown, Anthony R.; Avena, Nicole M.; Hoebel, Bartley G.

doi:10.1002/eat.20510

Cited by 22 publications

(17 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A recent study using the ABA model has demonstrated the efficacy of a HFD in rescuing rodents from anorexia (Brown et al, 2008). However, feeding a HFD to human AN patients runs contrary to the characteristics of the disorder and attempts to do this have been shown to heighten anxiety associated with eating a high-caloric diet (Boutelle, 1998).…”

Section: Discussionmentioning

confidence: 98%

The Cannabinoid Receptor Agonist THC Attenuates Weight Loss in a Rodent Model of Activity-Based Anorexia

Verty

Evetts

Crouch

et al. 2011

Neuropsychopharmacol

View full text Add to dashboard Cite

Anorexia nervosa (AN) is characterized by anhedonia whereby patients experience little pleasure or reward in many aspects of their lives. Reward pathways and the endocannabionid system have been implicated in the mediation of food intake. The potential to exploit these systems to reverse weight loss is investigated in a rodent model of activity-based anorexia (ABA). The effect of subchronic (6 days) Δ(9)-tetrahydrocannabinol (THC) treatment (0.1, 0.5, or 2.0 mg/kg/day) was assessed on chow and high-fat diet (HFD) intake, body weight, running wheel activity (RWA) as well as thermogenesis in brown adipose tissue (BAT) and lipid metabolism in white adipose tissue (WAT). Limited time availability of food and continuous access to running wheels led to anorexia and significantly reduced body weight. THC treatment (0.5 and 2.0 mg/kg/day) transiently stimulated chow intake with a moderate effect on RWA. THC (2.0 mg/kg/day) significantly reduced body weight loss and shifted markers of thermogenesis in BAT and lipid metabolism in WAT in directions consistent with reduced energy expenditure and lipolysis. THC (2.0 mg/kg/day) combined with HFD, produced a transient increase in food intake, reduction in RWA, attenuation of body weight loss, and changes in markers of thermogensis in BAT and lipolysis in the WAT. These changes were significantly greater than those seen in vehicle (HFD), vehicle (chow), and THC (chow)-treated animals. These data show for the first time the effectiveness of the endocannabinoid system in attenuating the weight loss associated with the development of ABA via a mechanism involving reduced energy expenditure.

show abstract

Section: Discussionmentioning

confidence: 98%

The Cannabinoid Receptor Agonist THC Attenuates Weight Loss in a Rodent Model of Activity-Based Anorexia

Verty

Evetts

Crouch

et al. 2011

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Currently, the first line of treatment for underweight patients with AN, is feeding and weight restoration, combined with psychotherapy. In ABA rats, certain palatable diets have been found to affect the development of, and recovery from, ABA (Brown et al ., ). Evidence for the efficacy of drug treatments for AN is limited, and currently there are no FDA or EMA approved drugs for the treatment of AN.…”

Section: Treatment Of An With Monoaminergic Agentsmentioning

confidence: 97%

Pharmacological manipulations in animal models of anorexia and binge eating in relation to humans

Gestel

Kostrzewa

Adan

et al. 2014

British J Pharmacology

View full text Add to dashboard Cite

Eating disorders, such as anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorders (BED), are described as abnormal eating habits that usually involve insufficient or excessive food intake. Animal models have been developed that provide insight into certain aspects of eating disorders. Several drugs have been found efficacious in these animal models and some of them have eventually proven useful in the treatment of eating disorders. This review will cover the role of monoaminergic neurotransmitters in eating disorders and their pharmacological manipulations in animal models and humans. Dopamine, 5‐HT (serotonin) and noradrenaline in hypothalamic and striatal regions regulate food intake by affecting hunger and satiety and by affecting rewarding and motivational aspects of feeding. Reduced neurotransmission by dopamine, 5‐HT and noradrenaline and compensatory changes, at least in dopamine D2 and 5‐HT2C/2A receptors, have been related to the pathophysiology of AN in humans and animal models. Also, in disorders and animal models of BN and BED, monoaminergic neurotransmission is down‐regulated but receptor level changes are different from those seen in AN. A hypofunctional dopamine system or overactive α2‐adrenoceptors may contribute to an attenuated response to (palatable) food and result in hedonic binge eating. Evidence for the efficacy of monoaminergic treatments for AN is limited, while more support exists for the treatment of BN or BED with monoaminergic drugs. Linked Articles This article is part of a themed section on Animal Models in Psychiatry Research. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-20

show abstract

“…Because dopamine is integral to mesolimbic reward processing, it follows logically that central reward dysfunction in AN and ABA is associated with the DA disturbances described above, specifically within the mesolimbic reward circuit. Indeed, rodent studies indicate that the ABA phenotype can be ameliorated by increasing the hedonic or rewarding value of food, by substituting laboratory chow with a high‐fat diet alone or combined with delta‐9‐thetrahydrocannabinol (THC) administration, both of which have effects mediated by DA signalling …”

Section: Dopamine and Reward Disruptions In Abamentioning

confidence: 99%

A focus on reward in anorexia nervosa through the lens of the activity‐based anorexia rodent model

Foldi

Milton

Oldfield

2017

J Neuroendocrinology

View full text Add to dashboard Cite

Patients suffering anorexia nervosa (AN) become anhedonic, unable or unwilling to derive normal pleasures and tend to avoid rewarding outcomes, most profoundly in food intake. The activity-based anorexia model recapitulates many of the pathophysiological and behavioural hallmarks of the human condition, including a reduction in food intake, excessive exercise, dramatic weight loss, loss of reproductive cycles, hypothermia and anhedonia, and therefore it allows investigation into the underlying neurobiology of anorexia nervosa. The use of this model has directed attention to disruptions in central reward neurocircuitry, which may contribute to disease susceptibility. The purpose of this review is to demonstrate the utility of this unique model to provide insight into the mechanisms of reward relevant to feeding and weight loss, which may ultimately help to unravel the neurobiology of anorexia nervosa and, in a broader sense, the foundation of reward-based feeding. K E Y W O R D Sactivity-based anorexia, animal models, anorexia nervosa, dopamine, mesolimbic reward pathways | ANOREXIA NERVOSA AS A NEUROBIOLOGICAL DISORDERAnorexia nervosa (AN) is a debilitating psychiatric disorder of complex aetiology that is characterised by a relentless pursuit of weight loss through extreme food restriction and excessive exercise, as well as high rates of chronicity, morbidity and mortality.1 AN is accompanied by physiological, biochemical and behavioural disturbances, including a diminished capacity to experience pleasure or reward. Figure 1A). A core aspect of this hypothesis is that "top-down" cognitive modulatory mechanisms exert control over "bottom-up" ap- | NEUROCIRCUITRY MODULATING REWARD AND INHIBITIONIt is likely that AN behaviours are encoded in limbic and cognitive circuits that fall into two categories. The first may be described as "limbic" and involves the amygdala and ventral striatum, as well as regions of the cerebral cortex, including the insula, anterior cingulate and prefrontal regions, which collectively coordinate the affective response to stimuli including food and feeding. The current terminology introduced by Berridge and Kringelbach 11 is that "liking" is the actual pleasure component of reward and "wanting" is the measure of motivation or incentive salience for a reward. The microstructure of neural circuits and transmitters coding for pleasure can be subdivided, in simplistic terms, into (i) those dopaminergic projections originating in the ventral tegmental area (VTA) and extending to the nucleus accumbens (NAc) which account for "wanting" and (ii) the activation of μ-opioid, In addition to the interaction between these two broad determinants of anorexic behaviour, mesolimbic reward and cortical control, there are clearly modulatory influences form other regions that impinge on such circuits. One of these involves serotonin released from neurones originating in the midbrain raphe nuclei, which can influence reward processing and anhedonic behaviours via actions directly on the VTA, indire...

show abstract

A high‐fat diet prevents and reverses the development of activity‐based anorexia in rats

Cited by 22 publications

References 46 publications

The Cannabinoid Receptor Agonist THC Attenuates Weight Loss in a Rodent Model of Activity-Based Anorexia

The Cannabinoid Receptor Agonist THC Attenuates Weight Loss in a Rodent Model of Activity-Based Anorexia

Pharmacological manipulations in animal models of anorexia and binge eating in relation to humans

A focus on reward in anorexia nervosa through the lens of the activity‐based anorexia rodent model

Contact Info

Product

Resources

About