Inhibiting Food Reward: Delay Discounting, Food Reward Sensitivity, and Palatable Food Intake in Overweight and Obese Women

Uncontrolled eating—in the general population—is characterized by overeating, hedonic hunger and being drawn towards palatable foods. Theoretically, it is the result of a strong food reward signal in relation to a poor ability to exert inhibitory control. How food consumption influences inhibitory control and food reward sensitivity, and how this relates to the continued urge to eat, remains unclear though. We used fMRI (N=40) in order to investigate the neural mechanism underlying food reward sensitivity and food-specific response inhibition (go-nogo task), by comparing women reporting high versus low/average uncontrolled eating across two sessions: during an inter-meal hunger state and after consumption of a high-caloric snack. We found no effects of individual differences in uncontrolled eating, food consumption, nor their interaction on food reward sensitivity. Differences in uncontrolled eating and food consumption did interact in modulating activity in the left superior occipital gyrus during response inhibition of non-food stimuli, an area previously associated with successful nogo- vs. go-trials. Yet, behavioural performance on the go-nogo task was not modulated by uncontrolled eating nor food consumption. Women with a low/average tendency for uncontrolled eating may need more cognitive resources to support successful response inhibition of non-food stimuli during food ‘go’ blocks in an inter-meal hunger state, whereas women with a high tendency for uncontrolled eating showed this after food consumption. Considering current and previous findings, it seems that individual differences in uncontrolled eating in healthy women have only limited influence on food reward sensitivity and food-related inhibitory control, whereas differences in weight status (e.g., obesity) may have more impact.

Download Full-text

Intranasal insulin decreases palatable food intake, increases satiety and enhances positive mood in women with obesity

Appetite ◽

10.1016/j.appet.2020.104891 ◽

2020 ◽

pp. 104891

Author(s):

Elizabeth Schneider ◽

Elizabeth Martin ◽

Jason M. Thomas ◽

Manfred Hallschmid ◽

Michelle Lee ◽

...

Keyword(s):

Food Intake ◽

Positive Mood ◽

Intranasal Insulin ◽

Palatable Food

Download Full-text

Cyfip1 Haploinsufficiency Increases Compulsive-Like Behavior and Modulates Palatable Food Intake in Mice: Dependence on Cyfip2 Genetic Background, Parent-of Origin, and Sex

G3 Genes|Genome|Genetics ◽

10.1534/g3.119.400470 ◽

2019 ◽

Vol 9 (9) ◽

pp. 3009-3022 ◽

Cited By ~ 5

Author(s):

Richard K. Babbs ◽

Jacob A. Beierle ◽

Qiu T. Ruan ◽

Julia C. Kelliher ◽

Melanie M. Chen ◽

...

Keyword(s):

Food Intake ◽

Genetic Background ◽

Palatable Food ◽

Parent Of Origin

Download Full-text

Appetite hormones and addiction

10.1093/med/9780198797746.003.0012 ◽

2018 ◽

Author(s):

David J. Nutt ◽

Liam J. Nestor

Keyword(s):

Eating Disorder ◽

Food Intake ◽

Food Consumption ◽

Neural Substrates ◽

Reward Sensitivity ◽

Substance Addiction ◽

Alcohol And Drugs ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

The Brain

Many of the same behavioural and brain disturbances observed in addiction are also seen in obesity and binge-eating disorder. This suggests that there are shared neural substrates between substance addiction and compulsive food consumption. Food intake and appetite are regulated by numerous appetite hormones that exert their effects through brain systems involved in reward sensitivity, stress, impulsivity, and compulsivity. There is now emerging evidence that appetite hormones (e.g. ghrelin, glucagon-like peptide-1, orexin) can modulate addictive behaviours (e.g. craving) and the intake of alcohol and drugs. Therefore, there is an emerging shift into a new field of testing drugs that affect appetite hormones and their receptors in the brain, and their use in regulating the brain mechanisms that lead to relapse in addiction disorders.

Download Full-text

Oleoylethanolamide decreases frustration stress-induced binge-like eating in female rats: a novel potential treatment for binge eating disorder

Neuropsychopharmacology ◽

10.1038/s41386-020-0686-z ◽

2020 ◽

Vol 45 (11) ◽

pp. 1931-1941 ◽

Cited By ~ 5

Author(s):

Adele Romano ◽

Maria Vittoria Micioni Di Bonaventura ◽

Cristina Anna Gallelli ◽

Justyna Barbara Koczwara ◽

Dorien Smeets ◽

...

Keyword(s):

Eating Disorder ◽

Nucleus Accumbens ◽

Food Intake ◽

Binge Eating ◽

Binge Eating Disorder ◽

Female Rats ◽

Early Gene ◽

Mrna Levels ◽

Palatable Food ◽

Brain Areas

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.

Download Full-text