Early life overfeeding alters palatable food intake in response to tail pinch stress in adulthood

Abstract Binge eating disorder (BED) is the most frequent eating disorder, for which current pharmacotherapies show poor response rates and safety concerns, thus highlighting the need for novel treatment options. The lipid-derived messenger oleoylethanolamide (OEA) acts as a satiety signal inhibiting food intake through the involvement of central noradrenergic and oxytocinergic neurons. We investigated the anti-binge effects of OEA in a rat model of binge-like eating, in which, after cycles of intermittent food restrictions/refeeding and palatable food consumptions, female rats show a binge-like intake of palatable food, following a 15-min exposure to their sight and smell (“frustration stress”). Systemically administered OEA dose-dependently (2.5, 5, and 10 mg kg−1) prevented binge-like eating. This behavioral effect was associated with a decreased activation (measured by mapping the expression of c-fos, an early gene widely used as a marker of cellular activation) of brain areas responding to stress (such as the nucleus accumbens and amygdala) and to a stimulation of areas involved in the control of food intake, such as the VTA and the PVN. These effects were paralleled, also, to the modulation of monoamine transmission in key brain areas involved in both homeostatic and hedonic control of eating. In particular, a decreased dopaminergic response to stress was observed by measuring dopamine extracellular concentrations in microdialysates from the nucleus accumbens shell, whereas an increased serotonergic and noradrenergic tone was detected in tissue homogenates of selected brain areas. Finally, a decrease in corticotropin-releasing factor (CRF) mRNA levels was induced by OEA in the central amygdala, while an increase in oxytocin mRNA levels was induced in the PVN. The restoration of a normal oxytocin receptor density in the striatum paralleled the oxytocinergic stimulation produced by OEA. In conclusion, we provide evidence suggesting that OEA might represent a novel potential pharmacological target for the treatment of binge-like eating behavior.

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A laboratory environment previously associated with a palatablediet can result in overfeeding in rats

Indian Journal of Animal Research ◽

10.18805/ijar.v0iof.4555 ◽

2016 ◽

Author(s):

Alma Gabriela Martínez ◽

Antonio López-Espinoza ◽

Patricia Josefina López-Uriarte ◽

Claudia Patricia Beltrán-Miranda ◽

Hugo Daniel Miguel-Gómez ◽

...

Keyword(s):

Food Intake ◽

Food Consumption ◽

Eating Behavior ◽

Behavioral Effects ◽

Laboratory Animals ◽

Palatable Food ◽

Laboratory Environment ◽

Enriched Environments

Enriched and non-enriched laboratory environments produce various biological and behavioral effects on laboratory animals. One of the most impacted aspects in this regard is eating behavior. We examined associations between enriched vs. non-enriched environments and palatable vs. non-palatable diets on food intake in rats. Experiment 1 demonstrated that there are no significant differences in palatable food consumption irrespective of whether rats were exposed to enriched or non-enriched environments (P>0.05). In contrast, experiment 2 demonstrated that a combination of exposure to either of these environments and palatable food is enough to produce overfeeding in rats (P less than 0.05). These outcomes in rats may offer significant inferences in regards to the regulation of eating behavior in humans.

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Hindbrain orexin 1 receptors influence palatable food intake, operant responding for food, and food-conditioned place preference in rats

Psychopharmacology ◽

10.1007/s00213-013-3248-9 ◽

2013 ◽

Vol 231 (2) ◽

pp. 419-427 ◽

Cited By ~ 34

Author(s):

Kristen Kay ◽

Eric M. Parise ◽

Nicole Lilly ◽

Diana L. Williams

Keyword(s):

Food Intake ◽

Conditioned Place Preference ◽

Place Preference ◽

Palatable Food ◽

Operant Responding

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DNA Methyltransferase 1 and 3a Expression in the Frontal Cortex Regulates Palatable Food Consumption

10.1101/2021.05.23.445176 ◽

2021 ◽

Author(s):

Mohan C Manjegowda ◽

Jonathan Joy-Gaba ◽

Eric R Wengert ◽

Anusha U Saga ◽

Daniel M Warthen ◽

...

Keyword(s):

Food Intake ◽

Food Consumption ◽

Dna Methyltransferase ◽

Drugs Of Abuse ◽

Pyramidal Cells ◽

Dna Methyltransferase 1 ◽

Palatable Food ◽

Neuronal Function ◽

Neuron Excitability ◽

Methyltransferase 1

DNA methylation is an important regulatory mechanism in the control of neuronal function. Both during development and following exposure to salient stimuli, plasticity in the methylation of cytosine residues leads to a change in neuron excitability that subsequently sculpts animal behavior. However, although the response of DNA methyltransferase enzymes in adult neurons to stimuli such as drugs of abuse have been described, less is known about how these enzymes regulate methylation at specific loci to change the drive to ingest natural rewards. Specifically, we do not understand how changes in methylation within important brain areas known to regulate palatable food intake can affect ingestion, while a detailed investigation of the neurophysiological and genomic effects of perturbing methyltransferase function has not been pursued. By deleting DNA methyltransferase 1 and 3a in the mouse prefrontal cortex, we observed the requirement for these enzymes in the regulation of nutrient rich food consumption in the absence of any effect on the intake of low fat and low sugar chow. We also determined that the deletion profoundly affected neuron excitability within pyramidal cells resident in superficial layers II/III of the cortex but had little effect in deep layer V neurons. Finally, reduced representation bisulfite sequencing revealed both hypo and hypermethylation in response to methyltransferase deletion, an effect that was observed in binding sites for retinoic acid receptor beta (RARβ) located within regulatory regions of genes known to affect neuronal function. Together, our data suggest that alterations in the actions of RARβ could shift neuronal activity to reduce palatable food intake.

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