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Nutrients Apr 2022Chronic circadian disruption (CCD), such as occurs during rotating shiftwork, and insufficient sleep are each independently associated with poor health outcomes,... (Randomized Controlled Trial)
Randomized Controlled Trial
Chronic circadian disruption (CCD), such as occurs during rotating shiftwork, and insufficient sleep are each independently associated with poor health outcomes, including obesity and glucose intolerance. A potential mechanism for poor health is increased energy intake (i.e., eating), particularly during the circadian night, when the physiological response to energy intake is altered. However, the contributions of CCD and insufficient sleep to subjective hunger, appetite, food preference, and appetitive hormones are not clear. To disentangle the influences of these factors, we studied seventeen healthy young adults in a 32-day in-laboratory study designed to distribute sleep, wakefulness, and energy intake equally across all phases of the circadian cycle, thereby imposing CCD. Participants were randomized to the Control (1:2 sleep:wake ratio, = 8) or chronic sleep restriction (CSR, 1:3.3 sleep:wake ratio, = 9) conditions. Throughout each waking episode the participants completed visual analog scales pertaining to hunger, appetite, and food preference. A fasting blood sample was collected to assess appetitive hormones. CCD was associated with a significant decrease in hunger and appetite in a multitude of domains in both the Control and CSR groups. This change in hunger was significantly correlated with changes in the ghrelin/leptin ratio. These findings further our understanding of the contributions of CCD and insufficient sleep on subjective hunger and appetite as well as of their possible contributions to adverse health behaviors.
Topics: Appetite; Food Preferences; Ghrelin; Humans; Hunger; Sleep; Sleep Deprivation; Young Adult
PubMed: 35565768
DOI: 10.3390/nu14091800 -
Nature Metabolism Jul 2022The overconsumption of highly caloric and palatable foods has caused a surge in obesity rates in the past half century, thereby posing a healthcare challenge due to the... (Review)
Review
The overconsumption of highly caloric and palatable foods has caused a surge in obesity rates in the past half century, thereby posing a healthcare challenge due to the array of comorbidities linked to heightened body fat accrual. Developing treatments to manage body weight requires a grasp of the neurobiological basis of appetite. In this Review, we discuss advances in neuroscience that have identified brain regions and neural circuits that coordinate distinct phases of eating: food procurement, food consumption, and meal termination. While pioneering work identified several hypothalamic nuclei to be involved in feeding, more recent studies have explored how neuronal populations beyond the hypothalamus, such as the mesolimbic pathway and nodes in the hindbrain, interconnect to modulate appetite. We also examine how long-term exposure to a calorically dense diet rewires feeding circuits and alters the response of motivational systems to food. Understanding how the nervous system regulates eating behaviour will bolster the development of medical strategies that will help individuals to maintain a healthy body weight.
Topics: Appetite; Body Weight; Diet; Feeding Behavior; Humans; Obesity
PubMed: 35879462
DOI: 10.1038/s42255-022-00611-y -
Neuroscience and Biobehavioral Reviews Sep 2017The brain-gut-axis is an interdependent system affecting neural functions and controlling our eating behaviour. In recent decades, neuroimaging techniques have... (Review)
Review
The brain-gut-axis is an interdependent system affecting neural functions and controlling our eating behaviour. In recent decades, neuroimaging techniques have facilitated its investigation. We systematically looked into functional and neurochemical brain imaging studies investigating how key molecules such as ghrelin, glucagon-like peptide-1 (GLP-1), peptide tyrosine-tyrosine (PYY), cholecystokinin (CCK), leptin, glucose and insulin influence the function of brain regions regulating appetite and satiety. Of the 349 studies published before July 2016 identified in the database search, 40 were included (27 on healthy and 13 on obese subjects). Our systematic review suggests that the plasma level of ghrelin, the gut hormone promoting appetite, is positively correlated with activation in the pre-frontal cortex (PFC), amygdala and insula and negatively correlated with activation in subcortical areas such as the hypothalamus. In contrast, the plasma levels of glucose, insulin, leptin, PYY, GLP-1 affect the same brain regions conversely. Our study integrates previous investigations of the gut-brain matrix during food-intake and homeostatic regulation and may be of use for future meta-analyses of brain-gut interactions.
Topics: Appetite; Brain; Gastrointestinal Tract; Hormones; Humans; Satiation
PubMed: 28669754
DOI: 10.1016/j.neubiorev.2017.06.013 -
JAMA Network Open Sep 2021Nonnutritive sweeteners (NNSs) are used as an alternative to nutritive sweeteners to quench desire for sweets while reducing caloric intake. However, studies have shown... (Randomized Controlled Trial)
Randomized Controlled Trial
IMPORTANCE
Nonnutritive sweeteners (NNSs) are used as an alternative to nutritive sweeteners to quench desire for sweets while reducing caloric intake. However, studies have shown mixed results concerning the effects of NNSs on appetite, and the associations between sex and obesity with reward and appetitive responses to NNS compared with nutritive sugar are unknown.
OBJECTIVE
To examine neural reactivity to different types of high-calorie food cues (ie, sweet and savory), metabolic responses, and eating behavior following consumption of sucralose (NNS) vs sucrose (nutritive sugar) among healthy young adults.
DESIGN, SETTING, AND PARTICIPANTS
In a randomized, within-participant, crossover trial including 3 separate visits, participants underwent a functional magnetic resonance imaging task measuring blood oxygen level-dependent signal in response to visual cues. For each study visit, participants arrived at the Dornsife Cognitive Neuroimaging Center of University of Southern California at approximately 8:00 am after a 12-hour overnight fast. Blood was sampled at baseline and 10, 35, and 120 minutes after participants received a drink containing sucrose, sucralose, or water to measure plasma glucose, insulin, glucagon-like peptide(7-36), acyl-ghrelin, total peptide YY, and leptin. Participants were then presented with an ad libitum meal. Participants were right-handed, nonsmokers, weight-stable for at least 3 months before the study visits, nondieters, not taking medication, and with no history of eating disorders, illicit drug use, or medical diagnoses. Data analysis was performed from March 2020 to March 2021.
INTERVENTIONS
Participants ingested 300-mL drinks containing either sucrose (75 g), sucralose (individually sweetness matched), or water (as a control).
MAIN OUTCOMES AND MEASURES
Primary outcomes of interest were the effects of body mass index (BMI) status and sex on blood oxygen level-dependent signal to high-calorie food cues, endocrine, and feeding responses following sucralose vs sucrose consumption. Secondary outcomes included neural, endocrine, and feeding responses following sucrose vs water and sucralose vs water (control) consumption, and cue-induced appetite ratings following sucralose vs sucrose (and vs water).
RESULTS
A total of 76 participants were randomized, but 2 dropped out, leaving 74 adults (43 women [58%]; mean [SD] age, 23.40 [3.96] years; BMI range, 19.18-40.27) who completed the study. In this crossover design, 73 participants each received water (drink 1) and sucrose (drink 2), and 72 participants received water (drink 1), sucrose (drink 2), and sucralose (drink 3). Sucrose vs sucralose was associated with greater production of circulating glucose, insulin, and glucagon-like peptide-1 and suppression of acyl-ghrelin, but no differences were found for peptide YY or leptin. BMI status by drink interactions were observed in the medial frontal cortex (MFC; P for interaction < .001) and orbitofrontal cortex (OFC; P for interaction = .002). Individuals with obesity (MFC, β, 0.60; 95% CI, 0.38 to 0.83; P < .001; OFC, β, 0.27; 95% CI, 0.11 to 0.43; P = .002), but not those with overweight (MFC, β, 0.02; 95% CI, -0.19 to 0.23; P = .87; OFC, β, -0.06; 95% CI, -0.21 to 0.09; P = .41) or healthy weight (MFC, β, -0.13; 95% CI, -0.34 to 0.07; P = .21; OFC, β, -0.08; 95% CI, -0.23 to 0.06; P = .16), exhibited greater responsivity in the MFC and OFC to savory food cues after sucralose vs sucrose. Sex by drink interactions were observed in the MFC (P for interaction = .03) and OFC (P for interaction = .03) after consumption of sucralose vs sucrose. Female participants had greater MFC and OFC responses to food cues (MFC high-calorie vs low-calorie cues, β, 0.21; 95% CI, 0.05 to 0.37; P = .01; MFC sweet vs nonfood cues, β, 0.22; 95% CI, 0.02 to 0.42; P = .03; OFC food vs nonfood cues, β, 0.12; 95% CI, 0.02 to 0.22; P = .03; and OFC sweet vs nonfood cues, β, 0.15; 95% CI, 0.03 to 0.27; P = .01), but male participants' responses did not differ (MFC high-calorie vs low-calorie cues, β, 0.01; 95% CI, -0.19 to 0.21; P = .90; MFC sweet vs nonfood cues, β, -0.04; 95% CI, -0.26 to 0.18; P = .69; OFC food vs nonfood cues, β, -0.08; 95% CI, -0.24 to 0.08; P = .32; OFC sweet vs nonfood cues, β, -0.11; 95% CI, -0.31 to 0.09; P = .31). A sex by drink interaction on total calories consumed during the buffet meal was observed (P for interaction = .03). Female participants consumed greater total calories (β, 1.73; 95% CI, 0.38 to 3.08; P = .01), whereas caloric intake did not differ in male participants (β, 0.68; 95% CI, -0.99 to 2.35; P = .42) after sucralose vs sucrose ingestion.
CONCLUSIONS AND RELEVANCE
These findings suggest that female individuals and those with obesity may be particularly sensitive to disparate neural responsivity elicited by sucralose compared with sucrose consumption.
TRIAL REGISTRATION
ClinicalTrials.gov Identifier: NCT02945475.
Topics: Adolescent; Adult; Appetite; Body Mass Index; California; Cross-Over Studies; Cues; Female; Humans; Male; Obesity; Reward; Sex Factors; Sucrose; Sweetening Agents; Young Adult
PubMed: 34581796
DOI: 10.1001/jamanetworkopen.2021.26313 -
Arquivos Brasileiros de Cardiologia Oct 2019
Topics: Aging; Appetite; Humans; Hypertension; Sodium Chloride; Sodium Chloride, Dietary
PubMed: 31621779
DOI: 10.5935/abc.20190186 -
Physiology & Behavior Sep 2021Food intake is tightly controlled by homeostatic signals sensitive to metabolic need for the regulation of body weight. This review focuses on the peripherally-secreted... (Review)
Review
Food intake is tightly controlled by homeostatic signals sensitive to metabolic need for the regulation of body weight. This review focuses on the peripherally-secreted gastrointestinal peptides (i.e., ghrelin, cholecystokinin, glucagon-like peptide 1, and peptide tyrosine tyrosine) that contribute to the control of appetite and discusses how these peptides or the signals arising from their release are disrupted in eating-related disorders across the weight spectrum, namely anorexia nervosa, bulimia nervosa, and obesity, and whether they are normalized following weight restoration or weight loss treatment. Further, the role of gut peptides in the pathogenesis and treatment response in human weight conditions as identified by rodent models are discussed. Lastly, we review the incretin- and hormone-based pharmacotherapies available for the treatment of obesity and eating-related disorders.
Topics: Appetite; Cholecystokinin; Eating; Ghrelin; Glucagon-Like Peptide 1; Peptide YY
PubMed: 33989649
DOI: 10.1016/j.physbeh.2021.113456 -
Peptides Apr 2021Hypoxia controls metabolism at several levels, e.g., via mitochondrial ATP production, glucose uptake and glycolysis. Hence it is likely that hypoxia also affects the... (Review)
Review
Hypoxia controls metabolism at several levels, e.g., via mitochondrial ATP production, glucose uptake and glycolysis. Hence it is likely that hypoxia also affects the action and/or production of many peptide hormones linked to food intake and appetite control. Many of those are produced in the gastrointestinal tract, endocrine pancreas, adipose tissue, and selective areas in the brain which modulate and concert their actions. However, the complexity of the hypoxia response and the links to peptides/hormones involved in food intake and appetite control in the different organs are not well known. This review summarizes the role of the hypoxia response and its effects on major peptides linked to appetite regulation, nutrition and metabolism.
Topics: Adipose Tissue; Appetite; Appetite Regulation; Cell Hypoxia; Eating; Energy Metabolism; Gastrointestinal Hormones; Glucose; Glycolysis; Humans; Leptin; Peptide Hormones
PubMed: 33577839
DOI: 10.1016/j.peptides.2021.170507 -
Biological Psychiatry May 2022The understanding of the neural control of appetite sheds light on the pathogenesis of eating disorders such as anorexia nervosa and obesity. Both diseases are a result... (Review)
Review
The understanding of the neural control of appetite sheds light on the pathogenesis of eating disorders such as anorexia nervosa and obesity. Both diseases are a result of maladaptive eating behaviors (overeating or undereating) and are associated with life-threatening health problems. The fine regulation of appetite involves genetic, physiological, and environmental factors, which are detected and integrated in the brain by specific neuronal populations. For centuries, the hypothalamus has been the center of attention in the scientific community as a key regulator of appetite. The hypothalamus receives and sends axonal projections to several other brain regions that are important for the integration of sensory and emotional information. These connections ensure that appropriate behavioral decisions are made depending on the individual's emotional state and environment. Thus, the mechanisms by which higher-order brain regions integrate exteroceptive information to coordinate feeding is of great importance. In this review, we will focus on the functional and anatomical projections connecting the hypothalamus to the limbic system and higher-order brain centers in the cortex. We will also address the mechanisms by which specific neuronal populations located in higher-order centers regulate appetite and how maladaptive eating behaviors might arise from altered connections among cortical and subcortical areas with the hypothalamus.
Topics: Appetite; Brain; Feeding and Eating Disorders; Humans; Hypothalamus; Obesity
PubMed: 34593204
DOI: 10.1016/j.biopsych.2021.07.015 -
British Journal of Pharmacology May 2021Given the high-energy requirements to sustain immune responses and healing processes, it is intriguing that lack of appetite (i.e., anorexia) is a cardinal feature of... (Review)
Review
Given the high-energy requirements to sustain immune responses and healing processes, it is intriguing that lack of appetite (i.e., anorexia) is a cardinal feature of sickness behaviour. While our understanding of the brain mechanisms that control appetite is rapidly growing, how inflammation affects these mechanisms is not fully understood. Here, we discuss advances in our understanding of discrete appetite controlling mechanisms and how inflammation influences their function. We further discuss the pathophysiological significance of anorexia and negative energy balance during the immune regulatory response. LINKED ARTICLES: This article is part of a themed issue on Cellular metabolism and diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.10/issuetoc.
Topics: Appetite; Brain; Humans; Immunity; Inflammation
PubMed: 32627171
DOI: 10.1111/bph.15189 -
Nutrients Jan 2023The objectives of this paper are to first present physiological and ecological aspects of the unique motivational state of sodium appetite, then to focus on systemic... (Review)
Review
The objectives of this paper are to first present physiological and ecological aspects of the unique motivational state of sodium appetite, then to focus on systemic physiology and brain mechanisms. I describe how laboratory protocols have been developed to allow the study of sodium appetite under controlled conditions, and focus on two such conditions specifically. The first of these is the presentation a sodium-deficient diet (SDD) for at least one week, and the second is accelerated sodium loss using SDD for 1-2 days coupled with the diuretic furosemide. The modality of consumption is also considered, ranging from a free intake of high concentration of sodium solution, to sodium-rich food or gels, and to operant protocols. I describe the pivotal role of angiotensin and aldosterone in these appetites and discuss whether the intakes or appetite are matched to the physiological need state. Several brain systems have been identified, most recently and microscopically using molecular biological methods. These include clusters in both the hindbrain and the forebrain. Satiation of sodium appetite is often studied using concentrated sodium solutions, but these can be consumed in apparent excess, and I suggest that future studies of satiation might emulate natural conditions in which excess consumption does not occur, using either SDD only as a stimulus, offering a sodium-rich food for the assessment of appetite, or a simple operant task.
Topics: Appetite; Sodium; Diuretics; Furosemide; Satiation; Sodium, Dietary
PubMed: 36771327
DOI: 10.3390/nu15030620