The potential role of and deficits in frontal cortical brain areas implicated in executive control of food intake

Moran, Timothy H.; Westerterp-Plantenga, Margriet S.

doi:10.1038/ijo.2011.249

Cited by 4 publications

(2 citation statements)

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“…Water intake was not affected by drug treatment in either group, suggesting that the effects are selective for feeding behavior. Frontal cortical areas of the brain have been implicated in the modulation of feeding behavior (Moran & Westerterp‐Plantenga ). A recent report has also shown that μ‐opioid receptors within the mPFC play an important role in driving overeating (Mena et al .…”

Section: Discussionmentioning

confidence: 99%

Opioid system in the medial prefrontal cortex mediates binge‐like eating

et al. 2013

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Binge eating disorder is an addiction-like disorder characterized by excessive food consumption within discrete periods of time. This study was aimed at understanding the role of the opioid system within the mPFC in the consummatory and motivational aspects of binge-like eating. For this purpose, we trained male rats to obtain either a sugary, highly palatable diet (Palatable rats) or a chow diet (Chow rats) for 1h a day. We then evaluated the effects of the opioid receptor antagonist, naltrexone, given either systemically or site-specifically into the NAcc or the mPFC on a fixed ratio 1 (FR1) and a progressive ratio schedule of reinforcement for food. Finally, we assessed the expression of the genes preOpioMelanoCortin (POMC), Pro-Dynorphin (PDyn), and Pro-Enkephalin (PEnk), coding for the opioids peptides in the NAcc and the mPFC in both groups. Palatable rats rapidly escalated their intake by 4 times. Naltrexone, when administered systemically and into the NAcc, reduced FR1 responding for food and motivation to eat under a progressive ratio in both Chow and Palatable rats; conversely, when administered into the mPFC, the effects were highly selective for binge eating rats. Furthermore, we found a two-fold increase in POMC and a ~50% reduction in PDyn gene expression in the mPFC of Palatable rats, when compared to control rats; however, no changes were observed in the NAcc. Our data suggest that neuroadaptations of the opioid system in the mPFC occur following intermittent access to highly palatable food, which may be responsible for the development of binge-like eating.

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Section: Discussionmentioning

confidence: 99%

Opioid system in the medial prefrontal cortex mediates binge‐like eating

et al. 2013

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“…Moreover, emerging functional neuroimaging evidence indicates the presence of hyper‐responsive neural networks that involve brain regions, such as the hypothalamus, ventromedial prefrontal cortex, and insula, as well as heightened reward circuitry activation in PWS in response to food stimulation [Dimitropoulos et al, ; Holsen et al, ; Mantoulan et al, ; Miller et al, ; Moran and Westerterp‐Plantenga, ; Ogura et al, ; Shapira et al, ]. Compared with body mass index (BMI)‐matched non‐PWS obese subjects, PWS subjects exhibited hyper‐activations in the subcortical reward circuitry and hypo‐activation in cortical inhibitory regions [Holsen et al, ].…”

Section: Introductionmentioning

confidence: 99%

Brain structural alterations in obese children with and withoutPrader‐Willi Syndrome

Zhang

Deneen

et al. 2017

Human Brain Mapping

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Prader-Willi syndrome (PWS) is a genetic imprinting disorder that is mainly characterized by hyperphagia and childhood obesity. Previous neuroimaging studies revealed that there is a significant difference in brain activation patterns between obese children with and without PWS. However, whether there are differences in the brain structure of obese children with and without PWS remains elusive. In the current study, we used T1-weighted and diffusion tensor magnetic resonance imaging to investigate alterations in the brain structure, such as the cortical volume and white matter integrity, in relation to this eating disorder in 12 children with PWS, 18 obese children without PWS (OB) and 18 healthy controls. Compared with the controls, both the PWS and OB groups exhibited alterations in cortical volume, with similar deficit patterns in 10 co-varying brain regions in the bilateral dorsolateral and medial prefrontal cortices, right anterior cingulate cortex, and bilateral temporal lobe. The white matter integrities of the above regions were then examined with an analysis method based on probabilistic tractography. The PWS group exhibited distinct changes in the reduced fractional anisotropy of white matter fibers connected to the co-varying regions, whereas the OB group did not. Our findings indicated that PWS and OB share similar gray matter alterations that are responsible for the development of eating disorders. Additionally, the distinct white matter alterations might explain the symptoms associated with food intake in PWS, including excessive hyperphagia and constant hunger. Hum Brain Mapp 38:4228-4238, 2017. © 2017 Wiley Periodicals, Inc.

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