Impaired Cross-Talk between Mesolimbic Food Reward Processing and Metabolic Signaling Predicts Body Mass Index

The anticipation of the pleasure derived from food intake drives the motivation to eat, and hence facilitate overconsumption of food which ultimately results in obesity. Brain imaging studies provide evidence that mesolimbic brain regions underlie both general as well as food related anticipatory reward processing. In light of this knowledge, the present study examined the neural responsiveness of the ventral striatum in participants with a broad BMI spectrum. The study differentiated between general (i.e. monetary) and food related anticipatory reward processing. We recruited a sample of volunteers with greatly varying body weights, ranging from a low BMI (below 20 kg/m²) over a normal (20 to 25 kg/m²) and overweight (25 to 30 kg/m²) BMI, to class I (30 to 35 kg/m² ) and class II (35 to 40 kg/m²) obesity. A total of 24 participants underwent functional magnetic resonance imaging whilst performing both a food and monetary incentive delay task, which allows to measure neural activation during the anticipation of rewards. After the presentation of a cue indicating the amount of food or money to be won, participants had to react correctly in order to earn snack points or money coins which could then be exchanged for real food or money, respectively, at the end of the experiment. During the anticipation of both types of rewards, participants displayed activity in the ventral striatum, a region that plays a pivotal role in the anticipation of rewards. Additionally, we observed that specifically anticipatory food reward processing predicted the individual BMI (current and maximum lifetime). This relation was found to be mediated by impaired hormonal satiety signaling, i.e. increased leptin levels and insulin resistance. These findings suggest that heightened food reward motivation contributes to obesity through impaired metabolic signaling

Familial Glucocorticoid Deficiency Type 1 due to a Novel Compound Heterozygous MC2R Mutation

Objective: Description of the clinical, biochemical and genetic features of a Polish patient with familial glucocorticoid deficiency. Methods: Detailed clinical investigation, hormonal analysis and sequencing of the coding region of the melanocortin 2 receptor (MC2R) gene in this patient. Results: We report on a 3-month-old boy with familial glucocorticoid deficiency who presented at the age of 3 months with skin hyperpigmentation, muscle weakness, mild jaundice and constipation. Hormonal analyses revealed high ACTH and TSH serum concentrations, low serum cortisol concentration along with normal blood electrolytes. On hydrocortisone supplementation, the disease symptoms disappeared and the child recovered completely. His physical and mental development progresses normally. Genetic analysis disclosed a novel compound heterozygous MC2R mutation p.Leu46fs and p.Val49Met. Conclusion: The heterozygous p.Leu46fs mutation adds to the small number of MC2R nonsense mutations and is the first frameshift mutation within the first transmembrane domain of the receptor. According to molecular modeling the Val49Met mutation results in a structural change of the first transmembrane domain and in a potential novel interaction of the transmembrane domains I and VII.Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich

Inhibitory Control and Hedonic Response towards Food Interactively Predict Success in a Weight Loss Programme for Adults with Obesity

Objective: Low inhibitory control and strong hedonic response towards food are considered to contribute to overeating and obesity. Based on previous research, the present study aimed at examining the potentially crucial interplay between these two factors in terms of long-term weight loss in people with obesity. Methods: BMI, inhibitory control towards food, and food liking were assessed in obese adults prior to a weight reduction programme (OPTIFAST® 52). After the weight reduction phase (week 13) and the weight loss maintenance phase (week 52), participants' BMI was re-assessed. Results: Baseline BMI, inhibitory control and food liking alone did not predict weight loss. As hypothesised, however, inhibitory control and food liking interactively predicted weight loss from baseline to week 13 and to week 52 (albeit the latter effect was less robust). Participants with low inhibitory control and marked food liking were less successful in weight reduction. Conclusion: These findings underscore the relevance of the interplay between cognitive control and food reward valuation in the maintenance of obesity

Inhibitory Control in Bulimic-Type Eating Disorders: A Systematic Review and Meta-Analysis

<div><p>The aim of this meta-analysis was to summarise data from neuropsychological studies on inhibitory control to general and disease-salient (i.e., food/eating, body/shape) stimuli in bulimic-type eating disorders (EDs). A systematic literature search was conducted to identify eligible experimental studies. The outcome measures studied included the performance on established inhibitory control tasks in bulimic-type EDs. Effect sizes (Hedges' <i>g</i>) were pooled using random-effects models. For inhibitory control to general stimuli, 24 studies were included with a total of 563 bulimic-type ED patients: 439 had bulimia nervosa (BN), 42 had anorexia nervosa of the binge/purge subtype (AN-b), and 82 had binge eating disorder (BED). With respect to inhibitory control to disease-salient stimuli, 12 studies were included, representing a total of 218 BN patients. A meta-analysis of these studies showed decreased inhibitory control to general stimuli in bulimic-type EDs (<i>g</i> = −0.32). Subgroup analysis revealed impairments with a large effect in the AN-b group (<i>g</i> = −0.91), impairments with a small effect in the BN group (<i>g</i> = −0.26), and a non-significant effect in the BED group (<i>g</i> = −0.16). Greater impairments in inhibitory control were observed in BN patients when confronted with disease-salient stimuli (food/eating: <i>g</i> = −0.67; body/shape: <i>g</i> = −0.61). In conclusion, bulimic-type EDs showed impairments in inhibitory control to general stimuli with a small effect size. There was a significantly larger impairment in inhibitory control to disease salient stimuli observed in BN patients, constituting a medium effect size.</p></div

Moderator analysis of studies on general inhibitory control in bulimic-type eating disorders.

<p>CI₉₅: 95% confidence interval, SE: standard error; BN: bulimia nervosa; BED: binge eating disorder; AN-b: anorexia nervosa from the binge/purge subtype; SST: Stop Signal Task; MFFT: Matching Familiar Figure Test; HSCT: Hayling Sentence Completion Test; SSIT: Simon Spatial Incompatibility Task; ELF: Excluded Letter Fluency test.</p

Description of studies on disease-related inhibitory control in bulimic-type eating disorders.

<p>BN: bulimia nervosa; BED: binge eating disorder; AN-b: anorexia nervosa of the binge/purge subtype; HC: healthy controls; BMI: body mass index;</p><p>^# : ideal body weight (percentage);</p><p>ns: no significant difference between patients and healthy controls;</p><p>significant group difference;</p><p>NR: not reported; RT: reaction time.</p

PRISMA Flow Chart.

<p>The flow chart highlights the number of articles found at each stage of the search and the final number of studies that were included in the review; *: the number of studies includes one outlier study; **: four articles reported data for inhibitory control to general stimuli and disease-salient stimuli.</p