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Review
. 2014 Oct;171(20):4767-84.
doi: 10.1111/bph.12789. Epub 2014 Sep 5.

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

Affiliations
Review

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

M A van Gestel et al. Br J Pharmacol. 2014 Oct.

Abstract

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-HT(2C/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.

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Figures

Figure 1
Figure 1
Example of 24 h behavioural data from one naïve male Wistar rat using automated monitoring system. Food intake was detected by automated weighing of the food hopper and water intake was measured by recording the animal’s contact with bottle nipple by lickometer. Each burst represents a meal or drinking session. Locomotor activity (counts) and core body temperature (°C) were measured by telemetric transmitters. All data were recorded to a computer. Dark bar represents the dark period (lights off, 16:00–04:00 h) and light bar represents the light period (lights on, 04:00–16:00 h).

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References

    1. Adam TC, Epel ES. Stress, eating and the reward system. Physiol Behav. 2007;91:449–458. - PubMed
    1. Ahlskog JE, Hoebel BG. Overeating and obesity from damage to a noradrenergic system in the brain. Science. 1973;182:166–169. - PubMed
    1. Alexander SPH, Benson HE, Faccenda E, Pawson AJ, Sharman JL. Spedding M, et al. The Concise Guide to PHARMACOLOGY 2013/14: G Protein-Coupled Receptors. Br J Pharmacol. 2013a;170:1459–1581. - PMC - PubMed
    1. Alexander SPH, Benson HE, Faccenda E, Pawson AJ, Sharman JL, Catterall WA, et al. The Concise Guide to PHARMACOLOGY 2013/14: Ligand-Gated Ion Channels. Br J Pharmacol. 2013b;170:1582–1606. - PMC - PubMed
    1. Alexander SPH, Benson HE, Faccenda E, Pawson AJ, Sharman JL. Spedding M, et al. The Concise Guide to PHARMACOLOGY 2013/14: Transporters. British Journal of Pharmacology. 2013c;170:1706–1796. - PMC - PubMed

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