GHS-R1a signaling in the DMH and VMH contributes to food anticipatory activity

Merkestein, Myrte; Gestel, M A van; Zwaal, Esther M. van der; Brans, Maike A.D.; Luijendijk, Mieneke C. M.; Rozen, A J van; Hendriks, Judith; Garner, Keith M.; Boender, Arjen J.; Pandit, Rahul; Adan, Roger A.H.

doi:10.1038/ijo.2013.131

Cited by 29 publications

(22 citation statements)

References 63 publications

(84 reference statements)

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“…The automated electronic food weighing system in rats gives continuous data from an animal's food intake and meal patterning (Tiesjema et al ., ; de Backer et al ., ; Janhunen et al ., 2011; 2013; la Fleur et al ., ; Merkestein et al ., ). A meal is defined as a feeding episode, for example, with a minimal consumption of 0.5 g chow and a 5 min intermeal interval, information is sent every 12 s to a computer.…”

Section: Monitoring Feeding Behaviour In Animalsmentioning

confidence: 97%

“…Another hormone of interest in the pathophysiology of AN that interacts with dopamine is ghrelin. Ghrelin GHS‐R1a receptors in the ventromedial hypothalamus (VMH) and dorsomedial hypothalamus were shown to mediate food‐anticipatory activity (Merkestein et al ., ). A diminished food‐anticipatory activity and unaltered food intake were observed after administration of a ghrelin receptor antagonist by an acute intracerebroventricular injection in rats or by chronic peripheral administration in mice (Verhagen et al ., ).…”

Section: Bridging Binge Eating To Its Animal Models With Dopaminementioning

confidence: 97%

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

Gestel

Kostrzewa

Adan

et al. 2014

British J Pharmacology

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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

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Section: Monitoring Feeding Behaviour In Animalsmentioning

confidence: 97%

Section: Bridging Binge Eating To Its Animal Models With Dopaminementioning

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

Self Cite

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“…FRW mice developed a light period activity close to the feeding time. This activity, usually called FAA, was also described in the ABA paradigm (23,48,49,68). The FAA is usually described 2-3 h before food distribution.…”

Section: E250mentioning

confidence: 99%

Physical activity: benefit or weakness in metabolic adaptations in a mouse model of chronic food restriction?

Méquinion

Caron

Zgheib

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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“…We followed the daily activation in the NTS and the arcuate nucleus of the hypothalamus (ARC), two‐first‐order structures providing input from the digestive system and the metabolic state directly to the SCN (Yi et al ., ; Buijs et al ., ), and second‐order structures that receive indirect metabolic information. We sampled the dorsomedial hypothalamic nucleus (DMH) and the intergeniculate leaflet (IGL), which also provide input to the SCN (Acosta‐Galvan et al ., ; Saderi et al ., ; Merkestein et al ., ). Present data show both an immediate effect of the LD cycle on some components of the circadian system and an immediate effect of digestive and metabolic signals on other structures suggesting that those two effects combined may underlie the accelerated re‐entrainment observed in general activity and temperature rhythms.…”

Section: Introductionmentioning

confidence: 97%

Scheduled meal accelerates entrainment to a 6‐h phase advance by shifting central and peripheral oscillations in rats

Ubaldo-Reyes

Buijs

Escobar

et al. 2017

Eur J of Neuroscience

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Travelling across several time zones requires a fast adjustment of the circadian system and the differential adjustment speeds of organs and systems results in what is commonly referred as jet lag. During this transitory state of circadian disruption, individuals feel discomfort, appetite loss, fatigue, disturbed sleep and deficient performance of multiple tasks. We have demonstrated that after a 6-h phase advance of the light-dark cycle (LD) scheduled food in phase with the new night onset can speed up re-entrainment. In this study, we explored the possible mechanisms underlying the fast re-entrainment due to the feeding schedule. We focused on first- and second-order structures that provide metabolic information to the suprachiasmatic nucleus (SCN). We compared (i) control rats without change in LD cycle; (ii) rats exposed to a 6-h phase advance of the LD cycle with food ad libitum; and (iii) rats exposed to the 6-h phase advance combined with food access in phase with the new night. We found an immediate synchronizing effect of food on stomach distention and on c-Fos expression in the nucleus of the solitary tract, arcuate nucleus of the hypothalamus, dorsomedial hypothalamic nucleus and paraventricular nucleus. These observations indicate that in a model of jet lag, scheduled feeding can favour an immediate shift in first- and second-order relays to the SCN and that by keeping feeding schedules coupled to the new night, a fast re-entrainment may be achieved by shifting peripheral and extra-SCN oscillations.

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GHS-R1a signaling in the DMH and VMH contributes to food anticipatory activity

Cited by 29 publications

References 63 publications

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

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

Physical activity: benefit or weakness in metabolic adaptations in a mouse model of chronic food restriction?

Scheduled meal accelerates entrainment to a 6‐h phase advance by shifting central and peripheral oscillations in rats

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