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Nature Metabolism Nov 2022Animals must adapt their dietary choices to meet their nutritional needs. How these needs are detected and translated into nutrient-specific appetites that drive...
Animals must adapt their dietary choices to meet their nutritional needs. How these needs are detected and translated into nutrient-specific appetites that drive food-choice behaviours is poorly understood. Here we show that enteroendocrine cells of the adult female Drosophila midgut sense nutrients and in response release neuropeptide F (NPF), which is an ortholog of mammalian neuropeptide Y-family gut-brain hormones. Gut-derived NPF acts on glucagon-like adipokinetic hormone (AKH) signalling to induce sugar satiety and increase consumption of protein-rich food, and on adipose tissue to promote storage of ingested nutrients. Suppression of NPF-mediated gut signalling leads to overconsumption of dietary sugar while simultaneously decreasing intake of protein-rich yeast. Furthermore, gut-derived NPF has a female-specific function in promoting consumption of protein-containing food in mated females. Together, our findings suggest that gut NPF-to-AKH signalling modulates specific appetites and regulates food choice to ensure homeostatic consumption of nutrients, providing insight into the hormonal mechanisms that underlie nutrient-specific hungers.
Topics: Female; Animals; Drosophila; Appetite; Sugars; Gastrointestinal Hormones; Drosophila Proteins; Mammals
PubMed: 36344765
DOI: 10.1038/s42255-022-00672-z -
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 -
Appetite Jan 2022
Topics: Appetite; Humans; Surveys and Questionnaires
PubMed: 34610394
DOI: 10.1016/j.appet.2021.105731 -
Current Opinion in Psychiatry Nov 2019The aim of this review is to describe animal models that simulate the features of eating disorders. The literature pertaining to animal models that are of relevance for... (Review)
Review
PURPOSE OF REVIEW
The aim of this review is to describe animal models that simulate the features of eating disorders. The literature pertaining to animal models that are of relevance for clinical eating disorders and the possible underpinning mechanisms was reviewed using PubMed, Ovid database and Google Scholar.
RECENT FINDINGS
New refinements of the circuits regulated by neurotransmitters and neuropeptides which instigate eating behaviours and the various feedback pathways which monitor acute and chronic nutrient status continue to be discovered. Moreover, work with the animal models that simulate the behavioural features and risk factors related to eating disorders is flourishing and providing new insights into possible causal mechanisms. For example, rodents develop binge-eating behaviours if they are intermittently exposed to processed, palatable foods and/or sugar adulterated drinks. This led to the controversial conceptualization of binge eating as a form of food addiction. Self-starvation taken to a fatal consequence such as occurs in anorexia nervosa can emerge in rodents exposed to triggers like social exclusion and/or the opportunity to exercise.
SUMMARY
There are plausible animal models for both anorexia nervosa and binge-eating disorders. These can be used to elaborate the theoretical models to explain the mechanisms underpinning eating disorders.
Topics: Animals; Appetite; Disease Models, Animal; Feeding Behavior; Feeding and Eating Disorders
PubMed: 31335333
DOI: 10.1097/YCO.0000000000000550 -
Gastroenterology Clinics of North... Jun 2023At usual weight, energy intake and expenditure are coupled and covary to maintain body weight (energy stores). A change in energy balance, especially weight loss,... (Review)
Review
At usual weight, energy intake and expenditure are coupled and covary to maintain body weight (energy stores). A change in energy balance, especially weight loss, invokes discoordinated effects on energy intake and output that favor return to previous weight. These regulatory systems reflect physiological changes in systems regulating energy intake and expenditure rather than a lack of resolve. The biological and behavioral physiology of dynamic weight change are distinct from those of attempts at static weight maintenance of an altered body weight. This suggests that optimal therapeutic approaches to losing or gaining vs. sustaining weight changes are different for most individuals.
Topics: Humans; Appetite; Obesity; Weight Loss; Energy Intake; Energy Metabolism
PubMed: 37197875
DOI: 10.1016/j.gtc.2023.03.004 -
The Journal of Physiology Mar 2022
Topics: Appetite; Appetite Regulation; Diet; Energy Intake
PubMed: 35288934
DOI: 10.1113/JP282727 -
Neurochemical Research Jan 2018Due to the biological importance of sodium and its relative scarcity within many natural environments, 'salt appetite' has evolved whereby dietary salt is highly sought... (Review)
Review
Due to the biological importance of sodium and its relative scarcity within many natural environments, 'salt appetite' has evolved whereby dietary salt is highly sought after and palatable when tasted. In addition to peripheral responses, salt depletion is detected within the brain via circumventricular organs and 11β-hydroxysteroid dehydrogenase type 2 (HSD2) neurons to increase salt appetite. Salt appetite is comprised of two main components. One component is the incentive salience or motivation for salt (i.e. how much salt is 'wanted'). Incentive salience is dynamic and largely depends on internal homeostatic conditions in combination with the detection of relevant cues. It involves the mesolimbic system and structures such as the central amygdala, and opioid signalling within these regions can increase salt intake in rodents. A second key feature is the hedonic palatability of salt (i.e. how much it is 'liked') when it is tasted. After detection on the tongue, gustatory information passes through the brainstem nucleus of the solitary tract and thalamus, before being consciously detected within the gustatory cerebral cortex. The positive or negative hedonic value of this stimulus is also dynamic, and is encoded by a network including the nucleus accumbens, ventral pallidum, and lateral parabrachial nucleus. Opioid signalling within these areas can alter salt intake, and 'liking'. The overconsumption of dietary salt likely contributes to hypertension and associated diseases, and hence further characterising the role played by opioid signalling has important implications for human health.
Topics: Analgesics, Opioid; Animals; Appetite; Brain; Humans; Motivation; Neurons; Sodium Chloride, Dietary
PubMed: 28646260
DOI: 10.1007/s11064-017-2336-3 -
Journal of Ethnopharmacology Feb 2015To understand the role of khat (Catha edulis) use on the aberrations in appetite and weight which are common comorbidities for khat and other amphetamine users. (Comparative Study)
Comparative Study Review
ETHNOPHARMACOLOGICAL RELEVANCE
To understand the role of khat (Catha edulis) use on the aberrations in appetite and weight which are common comorbidities for khat and other amphetamine users.
MATERIALS AND METHODS
We provide a comprehensive overview and conceptual summary of the historical cultural use of khat as a natural stimulant and describe the similarities and differences between cathinone (the main psychoactive constituent of khat) and amphetamine highlighting the limited literature on the neurophysiology of appetite and subsequent weight effects of khat.
RESULTS
Animal and some human studies indicate that khat produces appetite suppression, although little is known about mechanisms of this effect. Both direct and indirect effects of khat stem from multiple factors including behavioral, chemical and neurophysiological effects on appetite and metabolism. Classic and newly identified appetite hormones have not been explored sufficiently in the study of appetite and khat use. Unique methodological challenges and opportunities are encountered when examining effects of khat and cathinone including khat-specific medical comorbidities, unique route of administration, differential patterns of behavioral effects relative to amphetamines and the nascent state of our understanding of the neurobiology of this drug.
CONCLUSION
A considerable amount of work remains in the study of the appetite effects of khat chewing and outline a program of research that could inform our understanding of this natural amphetamine׳s appetite effects and help prepare health care workers for the unique health effects of this drug.
Topics: Alkaloids; Amphetamine; Animals; Appetite; Appetite Depressants; Catha; Humans; Plant Extracts; Plant Stems
PubMed: 25435289
DOI: 10.1016/j.jep.2014.11.002 -
Neuroscience and Biobehavioral Reviews Apr 2015Thirst and sodium appetite are the sensations responsible for the motivated behaviors of water and salt intake, respectively, and both are essential responses for the... (Review)
Review
Thirst and sodium appetite are the sensations responsible for the motivated behaviors of water and salt intake, respectively, and both are essential responses for the maintenance of hydromineral homeostasis in animals. These sensations and their related behaviors develop very early in the postnatal period in animals. Many studies have demonstrated several pre- and postnatal stimuli that are responsible for the developmental programing of thirst and sodium appetite and, consequently, the pattern of water and salt intake in adulthood in need-free or need-induced conditions. The literature systematically reports the involvement of dietary changes, hydromineral and cardiovascular challenges, renin-angiotensin system and steroid hormone disturbances, and lifestyle in these developmental factors. Therefore, this review will address how pre- and postnatal challenges can program lifelong thirst and sodium appetite in animals and humans, as well as which neuroendocrine substrates are involved. In addition, the possible epigenetic molecular mechanisms responsible for the developmental programing of drinking behavior, the clinical implications of hydromineral disturbances during pre- and postnatal periods, and the developmental origins of adult hydromineral behavior will be discussed.
Topics: Animals; Appetite; Brain; Drinking; Epigenesis, Genetic; Humans; Sodium, Dietary; Thirst
PubMed: 25528684
DOI: 10.1016/j.neubiorev.2014.12.012 -
Reviews in Endocrine & Metabolic... Sep 2014Glucagon-like peptide 1 (GLP-1) is a cleavage product of the pre-proglucagon gene which is expressed in the α-cells of the pancreas, the L-cells of the intestine, and... (Review)
Review
Glucagon-like peptide 1 (GLP-1) is a cleavage product of the pre-proglucagon gene which is expressed in the α-cells of the pancreas, the L-cells of the intestine, and neurons located in the caudal brainstem and hypothalamus. GLP-1 is of relevance to appetite and weight maintenance because it has actions on the gastrointestinal tract as well as the direct regulation of appetite. It delays gastric emptying and gut motility in humans. In addition, interventricular injections of GLP-1 inhibit food intake, independent of the presence of food in the stomach or gastric emptying. Peripherally administered GLP-1 also affects the central regulation of feeding. It is therefore the synergistic actions of GLP-1 in the gut and brain, acting on both central and peripheral receptors that seem responsible for the effects of the hormone on satiety.
Topics: Appetite; Body Weight; Eating; Gastric Emptying; Glucagon-Like Peptide 1; Humans
PubMed: 24811133
DOI: 10.1007/s11154-014-9289-5