scholarly journals The Role of “Mixed” Orexigenic and Anorexigenic Signals and Autoantibodies Reacting with Appetite-Regulating Neuropeptides and Peptides of the Adipose Tissue-Gut-Brain Axis: Relevance to Food Intake and Nutritional Status in Patients with Anorexia Nervosa and Bulimia Nervosa

2013 ◽  
Vol 2013 ◽  
pp. 1-21 ◽  
Author(s):  
Kvido Smitka ◽  
Hana Papezova ◽  
Karel Vondra ◽  
Martin Hill ◽  
Vojtech Hainer ◽  
...  

Eating disorders such as anorexia (AN) and bulimia nervosa (BN) are characterized by abnormal eating behavior. The essential aspect of AN is that the individual refuses to maintain a minimal normal body weight. The main features of BN are binge eating and inappropriate compensatory methods to prevent weight gain. The gut-brain-adipose tissue (AT) peptides and neutralizing autoantibodies play an important role in the regulation of eating behavior and growth hormone release. The mechanisms for controlling food intake involve an interplay between gut, brain, and AT. Parasympathetic, sympathetic, and serotoninergic systems are required for communication between brain satiety centre, gut, and AT. These neuronal circuits include neuropeptides ghrelin, neuropeptide Y (NPY), peptide YY (PYY), cholecystokinin (CCK), leptin, putative anorexigen obestatin, monoamines dopamine, norepinephrine (NE), serotonin, and neutralizing autoantibodies. This extensive and detailed report reviews data that demonstrate that hunger-satiety signals play an important role in the pathogenesis of eating disorders. Neuroendocrine dysregulations of the AT-gut-brain axis peptides and neutralizing autoantibodies may result in AN and BN. The circulating autoantibodies can be purified and used as pharmacological tools in AN and BN. Further research is required to investigate the orexigenic/anorexigenic synthetic analogs and monoclonal antibodies for potential treatment of eating disorders in clinical practice.

Author(s):  
Francesco Cavagnini

Appetite is regulated by a complex system of central and peripheral signals that interact in order to modulate eating behavior according the individual needs, i.e. the fasting or fed condition and the general nutritional status. Peripheral regulation includes adiposity signals and satiety signals, while central control is accomplished by several effectors, including the neuropeptidergic, monoaminergic and endocannabinoid systems. Adiposity signals inform the brain of the general nutritional status of the subject as indicated by the extent of fat depots. Indeed, leptin produced by the adipose tissue and insulin, whose pancreatic secretion tends to increase with the increase of fat mass, convey to the brain an anorexigenic message. Satiety signals, including cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), originate from the gastrointestinal tract during a meal and, through the vagus nerve, reach the nucleus tractus solitarius (NTS) in the caudal brainstem. From NTS afferents fibers project to the arcuate nucleus (ARC) of the hypothalamus, where satiety signals are integrated with adiposity signals and with several hypothalamic and supra-hypothalamic inputs, thus creating a complex network of neural circuits that finally elaborate the most appropriate response, in terms of eating behavior. In more detail, ARC neurons secrete a number of neuropeptides with orexigenic properties, such as neuropeptide Y (NPY) and agouti-related peptide (AGRP), or anorexigenic effects such as pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). Other brain areas involved in the control of food intake are located downstream the ARC: among these, the paraventricular nucleus (PVN), which produces anorexigenic peptides such as thyrotropin releasing hormone (TRH), corticotrophin releasing hormone (CRH) and oxytocin, the lateral hypothalamus (LHA) and perifornical area (PFA), secreting the orexigenic substances orexin-A (OXA) and melanin concentrating hormone (MCH). Recently, a great interest has developed for endogenous cannabinoids, important players in the regulation of food intake and energy metabolism. In the same context, increasing evidence is accumulating for a role played by the microbiota, the trillion of microorganism populating the human gastrointestinal tract. The complex interaction between the peripheral organs and the central nervous system has generated the concept of gut-brain axis, now incorporated into the physiology. A better understanding of the mechanisms governing the eating behavior will allow the development of drugs capable of reducing or enhancing food consumption.


2015 ◽  
Vol 6 ◽  
Author(s):  
Mohammed A. Islam ◽  
Ana B. Fagundo ◽  
Jon Arcelus ◽  
Zaida Agüera ◽  
Susana Jiménez-Murcia ◽  
...  

2017 ◽  
Author(s):  
Patricia Westmoreland ◽  
Phillip S Mehler

Feeding and eating disorders are defined by persistent disturbance of eating (or behaviors related to eating) with subsequent changes in consumption or absorption of nutrition that are detrimental to physical health and social functioning. The following eating disorders are described in the DSM-5: anorexia nervosa, bulimia nervosa, binge eating disorder, pica, rumination disorder, avoidant/restrictive food intake disorder (ARFID), other specified feeding or eating disorder (OSFED), and unspecified feeding or eating disorder (USFED). ARFID, OSFED, USFED, rumination disorder, and binge eating disorder are new additions to the manual and are first described in the DSM-5. The DSM-5 also provides severity specifiers—mild, moderate, severe, and extreme—for the diagnoses of bulimia nervosa and anorexia nervosa. This review describes the eating disorders enumerated in the DSM-5 and provides information regarding their genesis and course. This review contains 8 tables and 79 references Key words: avoidant/restrictive eating disorder, binge eating disorder, DSM-5, eating disorder, other specified feeding or eating disorder, pharmacotherapy, pica rumination, psychotherapy, unspecified feeding or eating disorder


2020 ◽  
Vol 15 (5) ◽  
pp. 87-92
Author(s):  
A.I. Khavkin ◽  
◽  
V.A. Ayrumov ◽  
N.O. Shvedkina ◽  
V.P. Novikova ◽  
...  

The increasing prevalence of alimentary obesity necessitates the search for its causes. In addition to eating disorders, other factors were found to affect lipid metabolism, including genetic predisposition, adipose tissue hormones, neurohormones, and digestive tract hormones regulating hunger and satiety, such as peptide YY (PYY) and ghrelin. This literature review focuses on these biologically active substances and their physiological and pathophysiological role. Key words: obesity, peptide, ghrelin


2017 ◽  
Author(s):  
Patricia Westmoreland ◽  
Phillip S Mehler

Feeding and eating disorders are defined by persistent disturbance of eating (or behaviors related to eating) with subsequent changes in consumption or absorption of nutrition that are detrimental to physical health and social functioning. The following eating disorders are described in the DSM-5: anorexia nervosa, bulimia nervosa, binge eating disorder, pica, rumination disorder, avoidant/restrictive food intake disorder (ARFID), other specified feeding or eating disorder (OSFED), and unspecified feeding or eating disorder (USFED). ARFID, OSFED, USFED, rumination disorder, and binge eating disorder are new additions to the manual and are first described in the DSM-5. The DSM-5 also provides severity specifiers—mild, moderate, severe, and extreme—for the diagnoses of bulimia nervosa and anorexia nervosa. This review describes the eating disorders enumerated in the DSM-5 and provides information regarding their genesis and course. This review contains 8 tables and 79 references Key words: avoidant/restrictive eating disorder, binge eating disorder, DSM-5, eating disorder, other specified feeding or eating disorder, pharmacotherapy, pica rumination, psychotherapy, unspecified feeding or eating disorder


Author(s):  
Beate M. Herbert ◽  
Olga Pollatos

The importance of interoception for adaptive and maladaptive behavior, as well as for psychopathology, has gained growing interest, and dysfunctional interoception has been recognized as representing a core impairment across psychosomatic and psychiatric disorders. Eating is intrinsically guided by interoceptive signals and is directly associated with homeostatic psychophysiological needs, well-being, and survival. This chapter provides conceptually and empirically drawn conclusions focusing on the relevance of distinguishable dimensions of interoception for shaping eating behavior and body weight, and for eating disorders. Going beyond eating behavior per se, anorexia and bulimia nervosa are conceptualized as characterized by profound impairment of the self, with dysfunctional interoception at its core. Predictive coding models are addressed to integrate conclusions and empirical findings tentatively.


1987 ◽  
Vol 150 (6) ◽  
pp. 777-781 ◽  
Author(s):  
J. Hubert Lacey ◽  
G. Smith

This study examines the impact of pregnancy on the reported eating behaviour of 20 untreated normal body weight bulimia nervosa women; it also reports foetal and obstetric abnormalities and indicates the initial eating habits of the infants. The prevalence of binge-eating and self-induced vomiting reduced sequentially during each trimester of pregnancy. By the third trimester 15 women (75%) had stopped all bulimic behaviour and in the remainder the disturbed eating was less severe. Symptoms tended to return in the Puerperium and in nearly half the sample abnormal eating was more disturbed after delivery than before conception. However, the improvement associated with the pregnancy described by seven patients was maintained and for five it appears to have been curative. The common fear among pregnant bulimics that their abnormal eating behaviour may damage their unborn child cannot be dispelled by this study; the incidence of foetal abnormality (including cleft palate and cleft lip), multiple pregnancies and obstetric complications (including breech presentation and surgical intervention) was high. The nutrition and development of the infants was good although three mothers (15%) reported slimming their babies down within the first year.


CNS Spectrums ◽  
2015 ◽  
Vol 20 (4) ◽  
pp. 391-400 ◽  
Author(s):  
Guido K. W. Frank

Over the past decade, brain imaging has helped to better define eating disorder–related brain circuitry. Brain research on gray matter (GM) and white matter (WM) volumes had been inconsistent, possibly due to the effects of acute starvation, exercise, medication, and comorbidity, but newer studies have controlled for such effects. Those studies suggest larger left medial orbitofrontal gyrus rectus volume in ill adult and adolescent anorexia nervosa after recovery from anorexia nervosa, and in adult bulimia nervosa. The orbitofrontal cortex is important in terminating food intake, and altered function could contribute to self-starvation. The right insula, which processes taste but also interoception, was enlarged in ill adult and adolescent anorexia nervosa, as well as adults recovered from the illness. The fixed perception of being fat in anorexia nervosa could be related to altered insula function. A few studies investigated WM integrity, with the most consistent finding of reduced fornix integrity in anorexia and bulimia nervosa—a limbic pathway that is important in emotion but also food intake regulation. Functional brain imaging using basic sweet taste stimuli in eating disorders during the ill state or after recovery implicated repeatedly reward pathways, including insula and striatum. Brain imaging that targeted dopamine-related brain activity using taste-reward conditioning tasks suggested that this circuitry is hypersensitive in anorexia nervosa, but hyporesponsive in bulimia nervosa and obesity. Those results are in line with basic research and suggest adaptive reward system changes in the human brain in response to extremes of food intake—changes that could interfere with normalization of eating behavior.


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