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Appetite Dec 2022Memory processes may have several roles in appetite regulation. Here we examine one such role, derived from the animal literature, in which satiety cues lead to the...
Memory processes may have several roles in appetite regulation. Here we examine one such role, derived from the animal literature, in which satiety cues lead to the inhibition of rewarding food-related memories. We tested this idea over three studies (n's of 58, 67, 50 respectively), by presenting participants with visual or verbal food cues, and asking them to describe what these foods were like to eat. This recollection task was undertaken hungry and sated. The resulting recollections were then coded and contrasted across state. Irrespective of state, participants took the same time to make their recollections, they were of similar length and included the same amount of sensory detail and affective content. However, in all three studies, sated recollections tended to include more reports about how filling a food would be. This increase in reports of food fillingness across state, was significantly correlated with increases in reports of stomach distension across state. While these results are consistent with the operation of memory inhibition, a further possibility is considered, whereby interoceptive satiety cues are integrated into food-related recollections (but not other recollections) to form a memory-inteorception-combination, thereby drawing attention to the consequences of eating when sated.
Topics: Animals; Cues; Food; Hunger; Reward; Satiation
PubMed: 36055461
DOI: 10.1016/j.appet.2022.106289 -
Neurogastroenterology and Motility Jan 2024Food intake is regulated by homeostatic and hedonic systems that interact in a complex neuro-hormonal network. Dysregulation in energy intake can lead to obesity (OB) or...
BACKGROUND
Food intake is regulated by homeostatic and hedonic systems that interact in a complex neuro-hormonal network. Dysregulation in energy intake can lead to obesity (OB) or anorexia nervosa (AN). However, little is known about the neurohormonal response patterns to food intake in normal weight (NW), OB, and AN.
MATERIAL & METHODS
During an ad libitum nutrient drink (Ensure®) test (NDT), participants underwent three pseudo-continuous arterial spin labeling (pCASL) MRI scans. The first scan was performed before starting the NDT after a > 12 h overnight fast (Hunger), the second after reaching maximal fullness (Satiation), and the third 30-min after satiation (postprandial fullness). We measured blood levels of ghrelin, cholecystokinin (CCK), glucagon-like peptide (GLP-1), and peptide YY (PYY) with every pCASL-MRI scan. Semiquantitative cerebral blood flow (CBF) maps in mL/100 gr brain/min were calculated and normalized (nCBF) with the CBF in the frontoparietal white matter. The hypothalamus (HT), nucleus accumbens [NAc] and dorsal striatum [DS] were selected as regions of interest (ROIs).
RESULTS
A total of 53 participants, 7 with AN, 17 with NW (body-mass index [BMI] 18.5-24.9 kg/m ), and 29 with OB (BMI ≥30 kg/m ) completed the study. The NW group had a progressive decrease in all five ROIs during the three stages of food intake (hunger, satiation, and post-prandial fullness). In contrast, participants with OB showed a minimal change from hunger to postprandial fullness in all five ROIs. The AN group had a sustained nCBF in the HT and DS, from hunger to satiation, with a subsequent decrease in nCBF from satiation to postprandial fullness. All three groups had similar hormonal response patterns with a decrease in ghrelin, an increase in GLP-1 and PYY, and no change in CCK.
CONCLUSION
Conditions of regulated (NW) and dysregulated (OB and AN) energy intake are associated with distinctive neurohormonal activity patterns in response to hunger, satiation, and postprandial fullness.
Topics: Humans; Hunger; Ghrelin; Anorexia Nervosa; Satiation; Obesity; Peptide YY; Cholecystokinin; Glucagon-Like Peptide 1; Postprandial Period
PubMed: 37926943
DOI: 10.1111/nmo.14695 -
Appetite Oct 2021There are well known phenotypic differences in sweet-liking across individuals, but it remains unknown whether these are related to broader underlying differences in...
There are well known phenotypic differences in sweet-liking across individuals, but it remains unknown whether these are related to broader underlying differences in interoceptive abilities (abilities to sense the internal state of the body). Here, healthy women (N = 64) classified as sweet likers (SLs) or sweet dislikers (SDs) completed a bimodal interoception protocol. A heartbeat tracking and a heartbeat discrimination task determined cardiac interoception; both were accompanied by confidence ratings. A water load task, where participants consumed water to satiation and then to maximum fullness was used to assess gastric interoceptive abilities. Motivational state, psychometric characteristics and eating behaviour were also assessed. SLs performed significantly better than SDs on both heartbeat tasks, independently of impulsivity, anxiety, depression, and alexithymia. No differences in metacognitive awareness and subjective interoceptive measures were found. With gastric interoception, SLs were more sensitive to stomach distention, and they ingested less water than SDs to reach satiety when accounting for stomach capacity. SLs also scored higher on mindful and intuitive eating scales and on emotional eating particularly in response to negative stimuli; emotional overeating was fully mediated via interoceptive performance. Overall, our data suggest the SL phenotype may reflect enhanced responsiveness to internal cues more broadly.
Topics: Awareness; Emotions; Feeding Behavior; Female; Heart Rate; Humans; Interoception; Satiation
PubMed: 33965436
DOI: 10.1016/j.appet.2021.105290 -
The American Journal of Gastroenterology Jul 2021Functional dyspepsia (FD) is a prevalent condition with multifactorial pathophysiology, including impaired gastric accommodation (GA), hypersensitivity to gastric... (Review)
Review
INTRODUCTION
Functional dyspepsia (FD) is a prevalent condition with multifactorial pathophysiology, including impaired gastric accommodation (GA), hypersensitivity to gastric distention, and delayed gastric emptying. Drink tests (DT) have been proposed as a potential biomarker for the presence and severity of gastric sensorimotor dysfunction. Thus, we aimed to summarize the state of knowledge on different DT and their potential as a biomarker for FD.
METHODS
A PubMed and MEDLINE search was conducted for English language articles, reviews, meta-analyses, case series, and randomized controlled trials, including also published meeting abstracts.
RESULTS
Several DT have been described in literature (e.g., different type of liquid, number of calories used, pace of drinking, and subject's awareness of the amount of liquid drunk). FD patients ingest significantly less volume in the different variants of the tests. The slow nutrient ("satiety drinking") test (SDT) studies show the most consistent separation between health and FD and correlation with GA. However, sensitivity to distention may be correlated with rapid DT. SDTs were used to evaluate the effect of several pharmacological agents, often showing concordance between their effects on GA and tolerated nutrient volume. This correlation was not found mainly for agents with central actions.
DISCUSSION
An SDT is a potential diagnostic biomarker in FD, reflecting GA. Additional studies are required to confirm its role as a predictive biomarker for treatment outcome in FD.
Topics: Biomarkers; Case-Control Studies; Diagnostic Techniques, Digestive System; Drinking Behavior; Drinking Water; Dyspepsia; Gastric Emptying; Humans; Nutrients; Satiation; Severity of Illness Index; Time Factors
PubMed: 33941747
DOI: 10.14309/ajg.0000000000001242 -
Obesity Reviews : An Official Journal... Aug 2021Despite obesity declared a disease, there still exists considerable weight stigma in both popular culture and health care, which negatively impacts policy making... (Review)
Review
Despite obesity declared a disease, there still exists considerable weight stigma in both popular culture and health care, which negatively impacts policy making regarding prevention and treatment. While viewed as a choice or a failure of willpower by many, evidence exists to challenge the argument that both weight gain and failure to achieve weight loss maintenance are the individuals' fault due to personal failure or lack of responsibility. In this article, we draw upon literature from obesity treatment, neuroscience, philosophy of mind, and weight stigma to challenge the commonly held beliefs that individuals are free to choose how much they can weigh, and achievement of long-term weight loss maintenance is completely subject to conscious choice. In reality, the regulation of hunger, satiety, energy balance, and body weight takes place in subcortical regions of the brain. Thus, hunger and satiety signals are generated in regions of the brain, which are not associated with conscious experience. This points towards biological determinism of weight and challenges ideas of willpower and resultant moralization regarding body weight regulation. In this article, we will thus argue that in the context of dysregulation of hunger and satiety contributing to the obesity epidemic, a wider discourse related to personal responsibility and the stigma of obesity is needed to enhance understanding, prevention, and treatment of this complex disease. Obesity is a chronic disease requiring personalized treatment. Lifestyle interventions alone may not be enough to achieve medically significant and sustained weight loss for many individuals with obesity. By understanding that obesity is not due to a lack of motivation or willpower, the availability and utilization of additional treatments or combination of treatments such as lifestyle, pharmacotherapy, and surgery are likely to improve the quality of life for many suffering with this disease.
Topics: Humans; Obesity; Quality of Life; Satiation; Weight Gain; Weight Loss
PubMed: 33977636
DOI: 10.1111/obr.13270 -
Nature Reviews. Endocrinology Aug 2022
Topics: Humans; Obesity; Satiety Response
PubMed: 35650333
DOI: 10.1038/s41574-022-00704-4 -
The Proceedings of the Nutrition Society Feb 2021The enteroendocrine system is located in the gastrointestinal (GI) tract, and makes up the largest endocrine system in the human body. Despite that, its roles and... (Review)
Review
The enteroendocrine system is located in the gastrointestinal (GI) tract, and makes up the largest endocrine system in the human body. Despite that, its roles and functions remain incompletely understood. Gut regulatory peptides are the main products of enteroendocrine cells, and play an integral role in the digestion and absorption of nutrients through their effect on intestinal secretions and gut motility. Several peptides, such as cholecystokinin, polypeptide YY and glucagon-like peptide-1, have traditionally been reported to suppress appetite following food intake, so-called satiety hormones. In this review, we propose that, in the healthy individual, this system to regulate appetite does not play a dominant role in normal food intake regulation, and that there is insufficient evidence to wholly link postprandial endogenous gut peptides with appetite-related behaviours. Instead, or additionally, top-down, hedonic drive and neurocognitive factors may have more of an impact on food intake. In GI disease however, supraphysiological levels of these hormones may have more of an impact on appetite regulation as well as contributing to other unpleasant abdominal symptoms, potentially as part of an innate response to injury. Further work is required to better understand the mechanisms involved in appetite control and unlock the therapeutic potential offered by the enteroendocrine system in GI disease and obesity.
Topics: Appetite; Appetite Regulation; Enteroendocrine Cells; Gastrointestinal Diseases; Gastrointestinal Hormones; Gastrointestinal Tract; Humans; Nutritional Physiological Phenomena; Obesity; Postprandial Period; Satiation
PubMed: 32364087
DOI: 10.1017/S0029665120006965 -
The Journal of Endocrinology Sep 2023The brain is tuned to integrate food-derived signals from the gut, allowing it to accurately adjust behavioral and physiological responses in accordance with nutrient... (Review)
Review
The brain is tuned to integrate food-derived signals from the gut, allowing it to accurately adjust behavioral and physiological responses in accordance with nutrient availability. A key element of gut-to-brain communication is the relay of neural cues via peripheral sensory neurons (PSN) which harbor functionally specialized peripheral endings innervating the muscular and mucosal layers of gastrointestinal (GI) tract organs. In this review, we detail the properties of GI tract innervating PSN and describe their roles in regulating satiation and glucose metabolism in response to food consumption. We discuss the complex anatomical organization of vagal and spinal PSN subtypes, their peripheral and central projection patterns, and describe the limitations of unselective lesion and ablation approaches to investigate them. We then highlight the recent identification of molecular markers that allow selective targeting of PSN subtypes that innervate GI tract organs. This has facilitated accurately determining their projections, monitoring their responses to gut stimuli, and manipulating their activity. We contend that these recent developments have significantly improved our understanding of PSN-mediated gut-to-brain communication, which may open new therapeutic windows for the treatment of metabolic disorders, such as obesity and type 2 diabetes.
Topics: Humans; Diabetes Mellitus, Type 2; Brain; Satiation; Vagus Nerve; Glucose; Gastrointestinal Tract
PubMed: 37343229
DOI: 10.1530/JOE-22-0320 -
Nutrition Reviews Dec 2020In the United States and Mexico, the obesity epidemic represents a significant public health problem. Although obesity is often attributed to a Western-style, high-fat... (Review)
Review
In the United States and Mexico, the obesity epidemic represents a significant public health problem. Although obesity is often attributed to a Western-style, high-fat diet and decreased activity, there is now compelling evidence that this, in part, occurs because of the developmental programming effects resulting from exposure to maternal overnutrition. Human and animal studies demonstrate that maternal obesity and high-fat diet result in an increased risk for childhood and adult obesity. The potential programming effects of obesity have been partly attributed to hyperphagia, which occurs as a result of increased appetite with reduced satiety neuropeptides or neurons. However, depending on maternal nutritional status during the nursing period, the programmed hyperphagia and obesity can be exacerbated or prevented in offspring born to obese mothers. The underlying mechanism of this phenomenon likely involves the plasticity of the appetite regulatory center and thus presents an opportunity to modulate feeding and satiety regulation and break the obesity cycle.
Topics: Animals; Appetite; Diet, High-Fat; Diet, Western; Female; Humans; Hyperphagia; Infant; Infant Nutritional Physiological Phenomena; Infant, Newborn; Maternal Nutritional Physiological Phenomena; Obesity; Obesity, Maternal; Overnutrition; Pregnancy; Satiation
PubMed: 33196091
DOI: 10.1093/nutrit/nuaa121 -
Cell Reports Oct 2023Oxytocin-expressing paraventricular hypothalamic neurons (PVN neurons) integrate afferent signals from the gut, including cholecystokinin (CCK), to adjust whole-body...
Oxytocin-expressing paraventricular hypothalamic neurons (PVN neurons) integrate afferent signals from the gut, including cholecystokinin (CCK), to adjust whole-body energy homeostasis. However, the molecular underpinnings by which PVN neurons orchestrate gut-to-brain feeding control remain unclear. Here, we show that mice undergoing selective ablation of PVN neurons fail to reduce food intake in response to CCK and develop hyperphagic obesity on a chow diet. Notably, exposing wild-type mice to a high-fat/high-sugar (HFHS) diet recapitulates this insensitivity toward CCK, which is linked to diet-induced transcriptional and electrophysiological aberrations specifically in PVN neurons. Restoring OT pathways in diet-induced obese (DIO) mice via chemogenetics or polypharmacology sufficiently re-establishes CCK's anorexigenic effects. Last, by single-cell profiling, we identify a specialized PVN neuronal subpopulation with increased κ-opioid signaling under an HFHS diet, which restrains their CCK-evoked activation. In sum, we document a (patho)mechanism by which PVN signaling uncouples a gut-brain satiation pathway under obesogenic conditions.
Topics: Mice; Animals; Oxytocin; Paraventricular Hypothalamic Nucleus; Analgesics, Opioid; Neurons; Satiation; Cholecystokinin
PubMed: 37864798
DOI: 10.1016/j.celrep.2023.113305