Ghrelin response to hedonic eating in underweight and short-term weight restored patients with anorexia nervosa

2017 ◽  
Vol 41 (S1) ◽  
pp. S550-S550
Author(s):  
G. Fico ◽  
A.M. Monteleone ◽  
M. Nigro ◽  
G. Patriciello ◽  
U. Volpe ◽  
...  

IntroductionRecently, anorexia nervosa (AN) has been conceptualized as a reward-related disorder, and brain imaging studies have shown functional and structural abnormalities in areas of the brain involved in reward processes in both acute and recovered AN patients. However, the role of endogenous biochemical mediators, such as Ghrelin, in the modulation of reward processes has been poorly investigated in this eating disorder.ObjectivesHedonic eating, that is the consumption of food exclusively for pleasure and not to maintain energy homeostasis, is a useful paradigm to investigate the physiology of food-related reward.AimsWe assessed the Ghrelin response to food-related reward in symptomatic AN women in order to further explore the modulation of reward processes in this severe and debilitating disorder.MethodsPlasma levels of Ghrelin were measured in 7 underweight and 7 recently weight-restored satiated AN patients before and after the ingestion of a favorite (hedonic eating) and non-favorite (non-hedonic eating) food. Ghrelin responses were compared it that of previously studied healthy controls.ResultsWe found that in satiated underweight patients with AN plasma Ghrelin levels progressively decreased after the exposure and the consumption of both the favorite and non-favorite food whereas in satiated weight-restored AN patients and satiated healthy controls plasma Ghrelin concentrations significantly increased after the exposure to the favorite food and after eating it, but decreased after the non-favorite food.ConclusionsThese results suggest a derangement in the Ghrelin modulation of food-related pleasurable and rewarding feelings, which might sustain the reduced motivation toward food intake of acute AN patients.Disclosure of interestThe authors have not supplied their declaration of competing interest.

2008 ◽  
Vol 93 (11) ◽  
pp. 4418-4421 ◽  
Author(s):  
Palmiero Monteleone ◽  
Cristina Serritella ◽  
Vassilis Martiadis ◽  
Pasquale Scognamiglio ◽  
Mario Maj

Introduction: Peptides of the gut-brain axis have a pivotal role in the regulation of energy homeostasis. Obestatin, a sibling of ghrelin derived from preproghrelin, is thought to oppose ghrelin effects on food intake. Because changes in ghrelin levels have been associated with anorexia nervosa (AN) and bulimia nervosa (BN), the investigation of obestatin production may further contribute to understanding the role of peripheral peptides in patients with eating disorders. Methods: In the present study, we measured circulating blood levels of obestatin and ghrelin and assessed their relationships with anthropometric and clinical measures in 20 AN patients, 21 BN patients, and 20 appropriate healthy controls. Results: Compared with healthy women, patients with BN showed no significant differences in plasma obestatin and ghrelin concentrations and in the ghrelin/obestatin ratio, whereas underweight AN patients displayed significantly increased circulating levels of both obestatin (P < 0.009) and ghrelin (P < 0.002) and an increased ghrelin/obestatin ratio (P < 0.04). Moreover, in AN women, positive correlations emerged between the ghrelin/obestatin ratio and current body weight and body mass index. Conclusions: Underweight AN patients are characterized by increased concentrations of ghrelin and obestatin and a higher ghrelin to obestatin ratio. No changes in circulating ghrelin or obestatin as well as in ghrelin to obestatin ratio seem to occur in acutely ill patients with BN. Although those changes likely reflect the physiological state of symptomatic AN individuals, they may also contribute to the pathophysiology of the disorder.


2016 ◽  
Vol 33 (S1) ◽  
pp. S161-S162
Author(s):  
M. Nigro ◽  
A.M. Monteleone ◽  
L. Steardo ◽  
G. Patriciello ◽  
V. Di Maso ◽  
...  

IntroductionSome temperament characteristics of personality seem to be modulated by oxytocin. Patients suffering from eating disorders (EDs) display aberrant personality traits.Objectives and aimsWe investigated the relationships between plasma oxytocin levels and personality dimensions of patients with anorexia nervosa (AN) and bulimia nervosa (BN) and compared them to those of healthy controls.MethodsPlasma oxytocin levels were measured in 23 women with AN, 27 women with BN and 19 healthy controls and assessed their personality traits by means of the Cloninger's Temperament and Character Inventory-Revised (TCI-R).ResultsAN patients showed plasma levels of the hormone significantly lower than BN and healthy controls. In healthy women, plasma oxytocin levels resulted significantly correlated negatively with novelty seeking scores and positively with both harm avoidance (HA) scores and the attachment subscale scores of the reward dependence: these correlations explained 82% of the variability in circulating oxytocin. In BN patients, plasma oxytocin resulted negatively correlated with HA, whereas no significant correlations emerged in AN patients.ConclusionsThese findings confirm a dysregulation of oxytocin secretion in AN but not in BN and show, for the first time, that the association of circulating oxytocin to patients’ temperament traits is totally lost in underweight patients with AN and partially lost or even inverted in women with BN. These findings suggest a role of oxytocin in certain deranged behaviours of ED patients, which are influenced by the subjects’ personality traits.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2001 ◽  
Vol 6 (2) ◽  
pp. 146-152 ◽  
Author(s):  
Debra K. Katzman ◽  
Bruce Christensen ◽  
Arlene R. Young ◽  
Robert B. Zipursky

2019 ◽  
Vol 128 (06/07) ◽  
pp. 388-394
Author(s):  
Helge Müller-Fielitz ◽  
Markus Schwaninger

AbstractThyroid hormone (TH) regulation is important for development, energy homeostasis, heart function, and bone formation. To control the effects of TH in target organs, the hypothalamus-pituitary-thyroid (HPT) axis and the tissue-specific availability of TH are highly regulated by negative feedback. To exert a central feedback, TH must enter the brain via specific transport mechanisms and cross the blood-brain barrier. Here, tanycytes, which are located in the ventral walls of the 3rd ventricle in the mediobasal hypothalamus (MBH), function as gatekeepers. Tanycytes are able to transport, sense, and modify the release of hormones of the HPT axis and are involved in feedback regulation. In this review, we focus on the relevance of tanycytes in thyrotropin-releasing hormone (TRH) release and review available genetic tools to investigate the physiological functions of these cells.


2017 ◽  
Vol 41 (S1) ◽  
pp. S56-S56
Author(s):  
C. Crisafulli

BackgroundIt's known that psychiatric disorders are caused to either environmental and genetics factors. Through the years several hypotheses were tested and many genes were screened for association, resulting in a huge amount of data available for the scientific community. Despite that, the molecular mechanics behind psychiatric disorders remains largely unknown. Traditional association studies may be not enough to pinpoint the molecular underpinnings of psychiatric disorder. We tried to applying a methodology that investigates molecular-pathway-analysis that takes into account several genes per time, clustered in consistent molecular groups and may successfully capture the signal of a number of genetic variations with a small single effect on the disease. This approach might reveal more of the molecular basis of psychiatric disorders.Methodsi)We collected data on studies available in literature for the studied disorder (e.g. Schizophrenia, Bipolar Disorder);ii)We extracted a pool of genes that are likely involved with the disease;iii)We used these genes as starting point to map molecular cascades function-linked. The molecular cascades are then analyzed and pathways and sub-pathways, possibly involved with them, are identified and tested for association.Results/discussionWe obtained interesting results. In particular, signals of enrichment (association) were obtained multiple times on the molecular pathway associated with the pruning activity and inflammation. Molecular mechanics related to neuronal pruning were focused as a major and new hypothesis for the pathophysiology of psychiatric disorders and the role of inflammatory events has been extensively investigated in psychiatry. intersting, inflammatory mechanics in the brain may also play a role in neuronal pruning during the early development of CNS.Disclosure of interestThe author has not supplied his declaration of competing interest.


Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 1018
Author(s):  
Caitlyn A. Mullins ◽  
Ritchel B. Gannaban ◽  
Md Shahjalal Khan ◽  
Harsh Shah ◽  
Md Abu B. Siddik ◽  
...  

Obesity prevalence is increasing at an unprecedented rate throughout the world, and is a strong risk factor for metabolic, cardiovascular, and neurological/neurodegenerative disorders. While low-grade systemic inflammation triggered primarily by adipose tissue dysfunction is closely linked to obesity, inflammation is also observed in the brain or the central nervous system (CNS). Considering that the hypothalamus, a classical homeostatic center, and other higher cortical areas (e.g. prefrontal cortex, dorsal striatum, hippocampus, etc.) also actively participate in regulating energy homeostasis by engaging in inhibitory control, reward calculation, and memory retrieval, understanding the role of CNS oxidative stress and inflammation in obesity and their underlying mechanisms would greatly help develop novel therapeutic interventions to correct obesity and related comorbidities. Here we review accumulating evidence for the association between ER stress and mitochondrial dysfunction, the main culprits responsible for oxidative stress and inflammation in various brain regions, and energy imbalance that leads to the development of obesity. Potential beneficial effects of natural antioxidant and anti-inflammatory compounds on CNS health and obesity are also discussed.


2017 ◽  
Vol 41 (S1) ◽  
pp. S410-S410
Author(s):  
R. Guijarro ◽  
M. Cerviño ◽  
P. Castrillo

Acceptance and commitment therapy (ACT) is a third-generation therapy that relates to human suffering as an inherent part of life in the human condition. Concerning personal values, ACT is focused on the acceptance of suffering, by doing away with the avoidance of things that cause us discomfort.The goal of the therapy is to make a person's reactions to suffering more flexible, working with the role of the symptoms rather than with the eliminating the symptoms themselves.This paper shows how the application of this therapy to a person with generalized anxiety disorder helps to reduce symptoms such as uncontrollable worrying, lack of concentration and muscular tension that these patients often suffer. The modification of symptoms has been measured by a single case study, where the symptoms are assessed by questionnaires before and after the treatment's application. Diagnosis was made according to the Diagnostic and Statistical Manual of Mental Disorders’ (DSM-IV) criteria.Disclosure of interestThe authors have not supplied their declaration of competing interest.


Endocrinology ◽  
2009 ◽  
Vol 150 (7) ◽  
pp. 3101-3109 ◽  
Author(s):  
Andrea Peier ◽  
Jennifer Kosinski ◽  
Kimberly Cox-York ◽  
Ying Qian ◽  
Kunal Desai ◽  
...  

Neuromedin U (NMU) and neuromedin S (NMS) are structurally related neuropeptides that have been reported to modulate energy homeostasis. Pharmacological data have shown that NMU and NMS inhibit food intake when administered centrally and that NMU increases energy expenditure. Additionally, NMU-deficient mice develop obesity, whereas transgenic mice overexpressing NMU are lean and hypophagic. Two high-affinity NMU/NMS receptors, NMUR1 and NMUR2, have been identified. NMUR1 is predominantly expressed in the periphery, whereas NMUR2 is predominantly expressed in the brain, suggesting that the effects of centrally administered NMU and NMS are mediated by NMUR2. To evaluate the role of NMUR2 in the regulation of energy homeostasis, we characterized NMUR2-deficient (Nmur2−/−) mice. Nmur2−/− mice exhibited a modest resistance to diet-induced obesity that was at least in part due to reduced food intake. Acute central administration of NMU and NMS reduced food intake in wild-type but not in Nmur2−/− mice. The effects on activity and core temperature induced by centrally administered NMU were also absent in Nmur2−/− mice. Moreover, chronic central administration of NMU and NMS evoked significant reductions in body weight and sustained reductions in food intake in mice. In contrast, Nmur2−/− mice were largely resistant to these effects. Collectively, these data demonstrate that the anorectic and weight-reducing actions of centrally administered NMU and NMS are mediated predominantly by NMUR2, suggesting that NMUR2-selective agonists may be useful for the treatment of obesity.


2017 ◽  
Vol 41 (S1) ◽  
pp. S283-S283
Author(s):  
F. Pellegrino ◽  
A.M. Monteleone ◽  
M. Nigro ◽  
V. Ruzzi ◽  
M. Cimino ◽  
...  

IntroductionAnorexia nervosa (AN) is characterized by dysregulated eating that leads to chronic malnutrition, which may be responsible for several physical complications, including endocrine alterations, such as hyperactivity of the hypothalamus-pituitary-adrenal (HPA) axis.ObjectivesSeveral studies have shown a dysregulation of the cortisol awakening response (CAR) in symptomatic AN patients. However, it has not been established if the deranged CAR of underweight AN patients is a primary phenomenon or an alteration secondary to malnutrition.AimsThe aim of this study was to explore the salivary CAR in both underweight and weight-restored patients with AN.MethodsWe recruited 59 women: 18 undernourished AN patients, 15 weight-restored AN women and 26 normal-weight healthy controls. Saliva samples were collected in the morning, immediately after awakening and after 15, 30 and 60 minutes, in order to measure saliva levels of cortisol. Participants filled in the state-trait anxiety inventory (STAI) to test their anxiety levels in the morning of the test.ResultsCompared to healthy controls, underweight AN patients showed an enhanced CAR whereas the weight recovered patients had a normal CAR. These results were not correlated with levels of anxiety.ConclusionsFor the first time, our results demonstrate that the deranged CAR found in acute AN patients is not present in weight-restored ones, suggesting that altered activity of the HPA axis of symptomatic AN patients is a state-dependent phenomenon.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2010 ◽  
Vol 298 (6) ◽  
pp. R1475-R1484 ◽  
Author(s):  
Thomas A. Lutz

Amylin is an important player in the control of nutrient fluxes. Amylin reduces eating via a meal size effect by promoting meal-ending satiation. This effect seems to depend on a direct action in the area postrema (AP), which is an area rich in amylin receptors. Subsequent to the activation of AP neurons, the neural signal is conveyed to the forebrain via relays involving the nucleus of the solitary tract (NTS) and the lateral parabrachial nucleus (lPBN) to the lateral hypothalamic area (LHA) and other hypothalamic nuclei. While the NTS and lPBN seem to be necessary for amylin's eating inhibitory effect, the role of the LHA has not yet been fully investigated. Amylin may also act as an adiposity signal. Plasma levels of amylin are higher in obese individuals, and chronic infusion of amylin into the brain reduces body weight gain and adiposity; chronic infusion of an amylin receptor antagonist into the brain increases body adiposity. Amylin increases energy expenditure in rats; this effect occurs under various experimental conditions after peripheral and central administration. Together, these animal data, but also clinical data in humans, indicate that amylin is a promising candidate for the treatment of obesity; effects are most pronounced when amylin is combined with leptin. Finally, recent findings indicate that amylin acts as a neurotrophic factor in specific brain stem areas. Whether this effect may be relevant under physiological conditions requires further studies.


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