Neuroendocrinology of reward in anorexia nervosa and bulimia nervosa: Beyond leptin and ghrelin

Berner, Laura A.; Brown, Tiffany A.; Lavender, Jason M.; Lopez, Emily; Wierenga, Christina E.; Kaye, Walter H.

doi:10.1016/j.mce.2018.10.018

Cited by 73 publications

(42 citation statements)

References 248 publications

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“…10 Neuroendocrines and peptides, such as fat cell-derived leptin or ghrelin from the gastric mucosa, stimulate or dampen brain dopamine response and alterations in this system, which could further alter food approach in AN and BN. 11,12 To date, however, those hypotheses rely mostly on basic research. Cytokines, markers of inflammatory processes, have been found altered, and meta-analyses indicate a pattern of elevated tumor necrosis factor-alpha in AN, whereas the data on other cytokines are somewhat mixed, with no alterations in BN.…”

Section: Neurochemical Studiesmentioning

confidence: 99%

The Neurobiology of Eating Disorders

Frank¹,

Shott²,

DeGuzman³

2019

Child and Adolescent Psychiatric Clinics of North America

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Section: Neurochemical Studiesmentioning

confidence: 99%

The Neurobiology of Eating Disorders

Frank¹,

Shott²,

DeGuzman³

2019

Child and Adolescent Psychiatric Clinics of North America

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“…The effects of PYY 3–36 are mostly mediated through agonism at Y2 receptors on neurons both in the gastrointestinal tract and in the central nervous system [ 2 ]. Translational research implicates the arcuate nucleus of the hypothalamus and certain brain stem regions as key areas of central appetite-regulating circuits influenced by PYY 3–36 [ 12 ]. Batterham et al [ 13 ] found that peripherally infused PYY 3–36 leads to a significant reduction in appetite and food intake in healthy, non-obese volunteers.…”

Section: Introductionmentioning

confidence: 99%

Peptide YY3–36 concentration in acute- and long-term recovered anorexia nervosa

et al. 2020

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Purpose The gut-brain axis could be a possible key factor in the pathophysiology of anorexia nervosa. The neuropeptide peptide YY 3-36 , secreted by endocrine L cells of the gastrointestinal tract, is a known regulator of appetite and food intake. The objective of this study was to investigate peptide YY 3-36 plasma concentrations at different stages of anorexia nervosa in a combined cross-sectional and longitudinal design to differentiate between effects of acute undernutrition and more enduring characteristics. Methods We measured fasting plasma peptide YY 3-36 concentrations in young patients with acute anorexia nervosa (n = 47) and long-term recovered patients (n = 35) cross-sectionally in comparison to healthy control participants (n = 58), and longitudinally over the course of inpatient treatment. Physical activity was controlled as it may modulate peptide YY secretion. Results There was no group difference in peptide YY 3-36 concentration among young acutely underweight anorexia nervosa patients, long-term recovered anorexia nervosa patients, and healthy control participants. Longitudinally, there was no change in peptide YY 3-36 concentration after short-term weight rehabilitation. For acute anorexia nervosa patients at admission to treatment, there was a negative correlation between peptide YY 3-36 concentration and body mass index. Conclusions The current study provides additional evidence for a normal basal PYY 3-36 concentration in AN. Future studies should study multiple appetite-regulating peptides and their complex interplay and also use research designs including a food challenge.

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“…Disturbances in central and peripheral molecules that promote (orexigenic mediators) or inhibit (anorectic mediators) feeding behavior to control appetite and body weight via the hypothalamus (Hyp) have been observed in AN patients (Monteleone, ; Tortorella et al, ). In addition, altered reward responses in areas of the mesocorticolimbic system might contribute to the behavioral pathology of AN (Avena & Bocarsly, ; Berner et al, ). This central system contains neural pathways that drive hedonic feeding and consists of subpopulations of dopaminergic neurons that originate from the ventral tegmental area (VTA) and pars compacta of the substantia nigra and project to limbic structures such as nucleus accumbens (NAcc), amygdala (Amy) hippocampus (Hipp), and prefrontal cortex (PFC) (Meye & Adan, ).…”

Section: Introductionmentioning

confidence: 99%

Impaired brain endocannabinoid tone in the activity‐based model of anorexia nervosa

Collu

Scherma

Piscitelli

et al. 2019

Intl J Eating Disorders

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Objective Despite the growing knowledge on the functional relationship between an altered endocannabinoid (eCB) system and development of anorexia nervosa (AN), to date no studies have investigated the central eCB tone in the activity‐based anorexia (ABA) model that reproduces key aspects of human AN. Method We measured levels of two major eCBs, anandamide (AEA) and 2‐arachidonoylglycerol (2‐AG), those of two eCB‐related lipids, oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), and the cannabinoid type‐1 receptor (CB1R) density in the brain of female ABA rats, focusing on areas involved in homeostatic and rewarding‐related regulation of feeding behavior (i.e., prefrontal cortex, nucleus accumbens, caudato putamen, amygdala, hippocampus and hypothalamus). Analysis was carried out also at the end of recovery from the ABA condition. Results At the end of the ABA induction phase, 2‐AG was significantly decreased in ABA rats in different brain areas but not in the caudato putamen. No changes were detected in AEA levels in any region, whereas the levels of OEA and PEA were decreased exclusively in the hippocampus and hypothalamus. Furthermore, CB1R density was decreased in the dentate gyrus of hippocampus and in the lateral hypothalamus. After recovery, both 2‐AG levels and CB1R density were partially normalized in some areas. In contrast, AEA levels became markedly reduced in all the analyzed areas. Discussion These data demonstrate an altered brain eCB tone in ABA rats, further supporting the involvement of an impaired eCB system in AN pathophysiology that may contribute to the maintenance of some symptomatic aspects of the disease.

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Neuroendocrinology of reward in anorexia nervosa and bulimia nervosa: Beyond leptin and ghrelin

Cited by 73 publications

References 248 publications

The Neurobiology of Eating Disorders

The Neurobiology of Eating Disorders

Peptide YY3–36 concentration in acute- and long-term recovered anorexia nervosa

Impaired brain endocannabinoid tone in the activity‐based model of anorexia nervosa

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