Coming to your senses : Effects of changes in olfactory and gustatory function on eating behavior and the brain

2021 ◽  
Author(s):  
Elbrich M. Postma
Keyword(s):  
Eating Behavior ◽  
Gustatory Function ◽  
The Brain

scholarly journals IL CONTROLLO NEUROENDOCRINO DEL COMPORTAMENTO ALIMENTARE

2020 ◽  
Author(s):  
Francesco Cavagnini
Keyword(s):  
Gastrointestinal Tract ◽  
Food Intake ◽  
Nutritional Status ◽  
Eating Behavior ◽  
Nucleus Tractus Solitarius ◽  
Peptide Yy ◽  
Releasing Hormone ◽  
Fat Depots ◽  
Adiposity Signals ◽  
The Brain

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.

scholarly journals The effect of an 8-week mindful eating intervention on anticipatory reward responses in the midbrain

2017 ◽  
Author(s):  
Lieneke K Janssen ◽  
Iris Duif ◽  
Anne EM Speckens ◽  
Ilke van Loon ◽  
Jeanne HM de Vries ◽  
...  
Keyword(s):  
Active Control ◽  
Eating Behavior ◽  
Monetary Reward ◽  
Controlled Study ◽  
Mindful Eating ◽  
Food Cues ◽  
Reward Anticipation ◽  
Compulsive Behaviors ◽  
Before And After ◽  
The Brain

AbstractObesity is a highly prevalent disease, usually resulting from chronic overeating. Accumulating evidence suggests that increased neural responses during the anticipation of high caloric food play an important role in overeating. A promising method to counteract enhanced food anticipation in overeating might be mindfulness-based interventions (MBIs). However, how MBIs can affect food reward anticipation neurally has never been studied. In this randomized, actively controlled study we aimed to investigate whether an 8-week mindful eating intervention decreases reward anticipation in striatal and midbrain reward regions. Using functional Magnetic Resonance Imaging, we tested 58 healthy subjects with a wide body mass index range (BMI: 19-35 kg/m2), who were motivated to change their eating behavior. During scanning they performed an incentive delay task, measuring neural reward anticipation responses to caloric and monetary cues before and after 8 weeks of mindful eating or educational cooking (active control). Relative to educational cooking (active control), mindful eating decreased reward anticipation responses to food, but not to monetary reward cues, in the midbrain, but not the striatum. The effects were specific to reward anticipation and did not extend to reward receipt. These results show that an 8-week mindful eating intervention may decrease the salience of food cues specifically, which could result in decreased food-cue triggered overeating on the long term.Significance statementMindfulness-based interventions have been shown effective in reducing disordered eating behavior in clinical as well as non-clinical populations. Here, we present the first randomized actively controlled study investigating the effects of mindfulness on reward anticipation in the brain. Using fMRI we show that midbrain responses to caloric, but not monetary, reward cues are reduced following an 8-week intervention of mindful eating relative to educational cooking (active control). Mindful eating interventions may thus be promising in counteracting reward cue-driven overeating, particularly in our obesogenic environment with food cues everywhere. Moreover, our data show that specific mindfulness-based interventions can target specific reward-cue responses in the brain, which might be relevant in other compulsive behaviors such as addiction.

scholarly journals Cerebral μ-opioid and CB1-receptor systems have distinct roles in human feeding behavior

2020 ◽  
Author(s):  
Tatu Kantonen ◽  
Tomi Karjalainen ◽  
Laura Pekkarinen ◽  
Janne Isojärvi ◽  
Kari Kalliokoski ◽  
...  
Keyword(s):  
Eating Behavior ◽  
Neural Pathways ◽  
Healthy Individuals ◽  
Palatable Food ◽  
Food Cues ◽  
Positron Emission ◽  
External Eating ◽  
Eating Styles ◽  
Pet Scans ◽  
The Brain

AbstractEating behavior varies greatly between healthy individuals, but the neurobiological basis of these trait-like differences in feeding remains unknown. Central μ-opioid receptors (MOR) and cannabinoid CB1-receptors (CB1R) regulate energy balance via multiple neural pathways, promoting food intake and reward. Because obesity and eating disorders have been associated with alterations in brain’s opioid and endocannabinoid signaling, the variation in MOR and CB1R systems could potentially underlie distinct eating behavior phenotypes, also in non-obese population. In this retrospective positron emission tomography (PET) study, we analyzed [11C]carfentanil PET scans of MORs from 92 healthy subjects (70 males and 22 females), and [18F]FMPEP-d2 scans of CB1Rs from 35 subjects (all males, all also included in the [11C]carfentanil sample). Eating styles were measured with the Dutch Eating Behavior Questionnaire (DEBQ). We found that lower cerebral MOR availability was associated with increase in external eating – individuals with low MORs reported being more likely to eat in response to environment’s palatable food cues. CB1R availability was negatively associated with multiple eating behavior traits. We conclude that although MORs and CB1Rs overlap anatomically and functionally in the brain, they have distinct roles in mediating individual feeding patterns.

scholarly journals Improvement in Uncontrolled Eating Behavior after Laparoscopic Sleeve Gastrectomy Is Associated with Alterations in the Brain–Gut–Microbiome Axis in Obese Women

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2924 ◽  
Author(s):  
Tien S. Dong ◽  
Arpana Gupta ◽  
Jonathan P. Jacobs ◽  
Venu Lagishetty ◽  
Elizabeth Gallagher ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Weight Loss ◽  
Sleeve Gastrectomy ◽  
Laparoscopic Sleeve Gastrectomy ◽  
Eating Behavior ◽  
Gut Microbiome ◽  
Resting State ◽  
Brain Magnetic Resonance Imaging ◽  
Brain Morphology ◽  
The Brain

Background: Bariatric surgery is proven to change eating behavior and cause sustained weight loss, yet the exact mechanisms underlying these changes are not clearly understood. We explore this in a novel way by examining how bariatric surgery affects the brain–gut–microbiome (BGM) axis. Methods: Patient demographics, serum, stool, eating behavior questionnaires, and brain magnetic resonance imaging (MRI) were collected before and 6 months after laparoscopic sleeve gastrectomy (LSG). Differences in eating behavior and brain morphology and resting-state functional connectivity in core reward regions were correlated with serum metabolite and 16S microbiome data. Results: LSG resulted in significant weight loss and improvement in maladaptive eating behaviors as measured by the Yale Food Addiction Scale (YFAS). Brain imaging showed a significant increase in brain volume of the putamen (p.adj < 0.05) and amygdala (p.adj < 0.05) after surgery. Resting-state connectivity between the precuneus and the putamen was significantly reduced after LSG (p.adj = 0.046). This change was associated with YFAS symptom count. Bacteroides, Ruminococcus, and Holdemanella were associated with reduced connectivity between these areas. Metabolomic profiles showed a positive correlation between this brain connection and a phosphatidylcholine metabolite. Conclusion: Bariatric surgery modulates brain networks that affect eating behavior, potentially through effects on the gut microbiota and its metabolites.

scholarly journals Brain Insulin Resistance at the Crossroads of Metabolic and Cognitive Disorders in Humans

2016 ◽  
Vol 96 (4) ◽  
pp. 1169-1209 ◽  
Author(s):  
Stephanie Kullmann ◽  
Martin Heni ◽  
Manfred Hallschmid ◽  
Andreas Fritsche ◽  
Hubert Preissl ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Eating Behavior ◽  
Insulin Action ◽  
Cognitive Disorders ◽  
Metabolic Effects ◽  
Pathological Feature ◽  
Brain Insulin ◽  
Maternal Metabolism ◽  
Brain Insulin Resistance ◽  
The Brain

Ever since the brain was identified as an insulin-sensitive organ, evidence has rapidly accumulated that insulin action in the brain produces multiple behavioral and metabolic effects, influencing eating behavior, peripheral metabolism, and cognition. Disturbances in brain insulin action can be observed in obesity and type 2 diabetes (T2D), as well as in aging and dementia. Decreases in insulin sensitivity of central nervous pathways, i.e., brain insulin resistance, may therefore constitute a joint pathological feature of metabolic and cognitive dysfunctions. Modern neuroimaging methods have provided new means of probing brain insulin action, revealing the influence of insulin on both global and regional brain function. In this review, we highlight recent findings on brain insulin action in humans and its impact on metabolism and cognition. Furthermore, we elaborate on the most prominent factors associated with brain insulin resistance, i.e., obesity, T2D, genes, maternal metabolism, normal aging, inflammation, and dementia, and on their roles regarding causes and consequences of brain insulin resistance. We also describe the beneficial effects of enhanced brain insulin signaling on human eating behavior and cognition and discuss potential applications in the treatment of metabolic and cognitive disorders.

APPLICATION OF BRAIN NEUROIMAGING TECHNOLOGIES FOR CHILDHOOD OBESITY

2021 ◽  
Vol 100 (6) ◽  
pp. 91-96
Author(s):  
O.A. Oleynik ◽  
◽  
D.A. Kudlay ◽  
Yu.G. Samoilova ◽  
M.V. Matveeva ◽  
...  
Keyword(s):  
Childhood Obesity ◽  
Literature Review ◽  
Children And Adolescents ◽  
Eating Behavior ◽  
Literature Search ◽  
Controlled Trials ◽  
Cochrane Central Register ◽  
Brain Functioning ◽  
Central Register ◽  
The Brain

The problem of obesity among children and adolescents is becoming more and more significant every year due to the increasing prevalence and its complications. Altered brain functioning is noted in obesity and contribute to eating behavior as well as the brain-gastrointestinal tractvisceral fat axis. This literature review is focuses on the issues of neuroimaging studies of the brain in obesity in childhood and the possibilities of various methods in the diagnosis and prediction of disorders. Medline and Cochrane Central Register of Controlled Trials (CENTRAL) databases from 2000 to 2021 were used for the literature search.

A review of the neurobiology of obesity and the available pharmacotherapies

CNS Spectrums ◽  
2017 ◽  
Vol 22 (S1) ◽  
pp. 29-38 ◽  
Author(s):  
Mehala Subramaniapillai ◽  
Roger S. McIntyre
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Energy Balance ◽  
Physical Health ◽  
Food Consumption ◽  
Eating Behavior ◽  
Reward System ◽  
The Central Nervous System ◽  
Treatment Mechanisms ◽  
The Brain

Obesity is becoming an increasing problem worldwide. In addition to causing many physical health consequences, there is increasing evidence demonstrating that obesity is toxic to the brain and, as such, can be considered a disease of the central nervous system. Peripheral level regulators of appetite, such as leptin, insulin, ghrelin, and cholecystokinin, feed into the appetite center of the brain, which is controlled by the hypothalamus, to maintain homeostasis and energy balance. However, food consumption is not solely mediated by energy balance, but is also regulated by the mesolimbic reward system, where motivation, reward, and reinforcement factors influence obesity. The purpose of this review is to highlight the neurobiology of eating behavior and obesity and to describe various neurobiological treatment mechanisms to treat obesity.

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