Regulating Satiety in Bulimia Nervosa: The Role of Cholecystokinin

Hannon-Engel, Sandy

doi:10.1111/j.1744-6163.2011.00304.x

Cited by 10 publications

(4 citation statements)

References 58 publications

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“…Patients with BN have diminished release of CCK following ingestion of a standardized test meal [187, 206] (Table 2). It has been suggested that the decreased CCK response to a meal may play a role in diminished postingestive satiety observed in BN and that may contribute to the perpetuation and frequent relapse of this disorder [207, 208] (Table 2). …”

Section: An Overview Of Hunger-satiety Signals and Autoantibodies mentioning

confidence: 99%

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

Smitka

Papežová

Vondra

et al. 2013

International Journal of Endocrinology

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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.

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Section: An Overview Of Hunger-satiety Signals and Autoantibodies mentioning

confidence: 99%

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

Smitka

Papežová

Vondra

et al. 2013

International Journal of Endocrinology

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“…Several studies found that intravenously administered CCK causes a reduction in food intake of up to 16% in lean and higher weight participants (Cummings & Overduin, 2007 ; Gibbs et al, 1973 ; Murphy et al, 2006 ). In contrast, people with bulimia have low CCK plasma levels and respond poorly to administration of CCK (Geracioti et al, 1989 ; Hadley & Walsh, 2003 ; Hannon‐Engel, 2012 ).…”

Section: Physiology and Brain Systems Underlying Food Choicesmentioning

confidence: 99%

How we decide what to eat: Toward an interdisciplinary model of gut–brain interactions

Plaßmann

Schelski

Simon

et al. 2021

WIRES Cognitive Science

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Everyday dietary decisions have important short-term and long-term consequences for health and well-being. How do we decide what to eat, and what physiological and neurobiological systems are involved in those decisions? Here, we integrate findings from thus-far separate literatures: (a) the cognitive neuroscience of dietary decision-making, and (b) growing evidence of gutbrain interactions and especially influences of the gut microbiome on diet and health outcomes. We review findings that suggest that dietary decisions and food consumption influence nutrient sensing, homeostatic signaling in the gut, and the composition of the gut microbiome. In turn, the microbiome can influence host health and behavior. Through reward signaling pathways, the microbiome could potentially affect food and drink decisions. Such bidirectional links between gut microbiome and the brain systems underlying dietary decision-making may lead to self-reinforcing feedback loops that determine long-term dietary patterns, body mass, and health outcomes.

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“…For example, cholecystokinin and plasma peptide tyrosine tyrosine are important satiating hormones, which mainly respond to protein and fat consumption. 166 , 167 The roles of fat and protein intake have been less explored in the context of appetite regulation, 168 , 169 and further work is needed on this topic. This has relevance to the treatment of eating disorders, as it has been described that protein intake is low in this patient population.…”

Section: Effects Of Ultra-processed Foods On the Brainmentioning

confidence: 99%

The Western diet: a blind spot of eating disorder research?—a narrative review and recommendations for treatment and research

Ayton

Ibrahim

2019

Nutrition Reviews

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Over the last 50 years, in parallel with the obesity epidemic, the prevalence of eating disorders has increased and presentations have changed. In this narrative review, we consider recent research exploring the implications of changing patterns of food consumption on metabolic and neurobiological pathways, a hitherto neglected area in eating disorder research. One of the major changes over this time has been the introduction of ultra-processed (NOVA-4) foods, which are gradually replacing unprocessed and minimally processed foods. This has resulted in the increased intake of various sugars and food additives worldwide, which has important metabolic consequences: triggering insulin and glucose response, stimulating appetite, and affecting multiple endocrine and neurobiological pathways, as well as the microbiome. A paradigm shift is needed in the conceptual framework by which the vulnerability to, and maintenance of, different eating disorders may be understood, by integrating recent knowledge of the individual metabolic responses to modern highly processed foods into existing psychological models. This could stimulate research and improve treatment outcomes.

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Regulating Satiety in Bulimia Nervosa: The Role of Cholecystokinin

Cited by 10 publications

References 58 publications

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

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

How we decide what to eat: Toward an interdisciplinary model of gut–brain interactions

The Western diet: a blind spot of eating disorder research?—a narrative review and recommendations for treatment and research

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