IMBICE   05372
INSTITUTO MULTIDISCIPLINARIO DE BIOLOGIA CELULAR
Unidad Ejecutora - UE
artículos
Título:
Considerations about rodent models of binge eating episodes
Autor/es:
PERELLO M; VALDIVIA S; GARCÍA ROMERO G; RAINGO J
Revista:
Frontiers in psychology
Editorial:
Pully, Switzerland : Frontiers Research Foundation
Referencias:
Año: 2014 vol. 5 p. 1 - 4
Resumen:
A binge eating episode is defined as an uncontrolled
event of hyperphagia, in which people quickly eat a large amount of food
while feeling a sense of loss of control over eating (Wolfe et al., 2009).
Binge eating episodes are observed in a variety of human disorders
including bulimia nervosa (BN), binge eating disorder (BED), and the
binge/purge subtype of anorexia nervosa (AN) (Berger and Tanofsky-Kraff, 2012).
Binge eating episodes are also present in overweight and obese people,
as well as non-clinical populations under specific circumstances such as
stress. The etiology of this behavior is currently unknown. The use of
rodent models has been essential for understanding the pathogenesis of
many human diseases; however, it is challenging to mimic all features of
human binge eating in rodent models (Corwin and Buda-Levin, 2004; Perello et al., 2010a).
In particular, these models should not only display the objective
characteristics of a binge eating episode, namely the consumption of a
large amount of food in a short period of time, but also the subjective
characteristics of the feeling of loss of control.
Recently, we examined the neuronal circuitries activated
in naïve mice allowed to spontaneously eat a high fat diet (HFD) pellet
for 2 h (Valdivia et al., 2014).
We found that satiated mice with free access to regular chow rapidly
consume a significant amount of HFD when exposed to it, and that HFD
intake recruits centers of the mesolimbic pathway, which are known to be
activated in human beings displaying binge eating behavior (see below).
Experts in the field agreed that our simple model of HFD
overconsumption could be relevant for studying neuronal aspects of binge
eating behaviors. However, some reviewers argued that it was misleading
to describe our model as a model of binge eating. Some criticisms were
that our model lacked indications of feelings of loss of control,
repeated feeding episodes, escalation of intake over time, a significant
level of hyperphagia, and evidence that bingeing occurred in the face
of aversive consequences. The notable divergence in the opinion of the
journal's reviewers made evident that a comprehensive debate about
rodent binge eating models is needed. Here, we briefly present our
opinion about the features that a rodent model should fulfill in order
to be considered a reasonable model of binge eating episodes and its
implications in terms of the neuronal circuits involved.