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(1) Background: We examined the effect of the acute administration of olive oil (EVOO), linseed oil (GLO), soybean oil (SO), and palm oil (PO) on gastric motility and appetite in rats. (2) Methods: We assessed food intake, gastric retention (GR), and gene expression in all groups. (3) Results: Both EVOO and GLO were found to enhance the rate of stomach retention, leading to a decrease in hunger. On the other hand, the reduction in food intake caused by SO was accompanied by delayed effects on stomach retention. PO caused an alteration in the mRNA expression of NPY, POMC, and CART. Although PO increased stomach retention after 180 min, it did not affect food intake. It was subsequently verified that the absence of an autonomic reaction did not nullify the influence of EVOO in reducing food consumption. Moreover, in the absence of parasympathetic responses, animals that received PO exhibited a significant decrease in food consumption, probably mediated by lower NPY expression. (4) Conclusions: This study discovered that different oils induce various effects on parameters related to food consumption. Specifically, EVOO reduces food consumption primarily through its impact on the gastrointestinal tract, making it a recommended adjunct for weight loss. Conversely, the intake of PO limits food consumption in the absence of an autonomic reaction, but it is not advised due to its contribution to the development of cardiometabolic disorders.
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Regulação do Apetite , Hipotálamo , Neuropeptídeo Y , Azeite de Oliva , Óleo de Palmeira , Óleo de Soja , Nervo Vago , Animais , Nervo Vago/efeitos dos fármacos , Nervo Vago/fisiologia , Hipotálamo/metabolismo , Hipotálamo/efeitos dos fármacos , Masculino , Azeite de Oliva/farmacologia , Neuropeptídeo Y/genética , Neuropeptídeo Y/metabolismo , Óleo de Palmeira/farmacologia , Regulação do Apetite/efeitos dos fármacos , Óleo de Soja/administração & dosagem , Óleo de Soja/farmacologia , Ratos Wistar , Óleo de Semente do Linho/farmacologia , Ratos , Ingestão de Alimentos/efeitos dos fármacos , Óleos de Plantas/farmacologia , Pró-Opiomelanocortina/genética , Pró-Opiomelanocortina/metabolismo , Proteínas do Tecido Nervoso/genética , Proteínas do Tecido Nervoso/metabolismo , Motilidade Gastrointestinal/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , RNA Mensageiro/metabolismo , RNA Mensageiro/genéticaRESUMO
Successful weight management represents a challenge to obesity control. Evidence suggests that nut consumption promotes a prolonged satiety response. Therefore, we hypothesize that nuts could be associated with greater weight loss in comparison to a control group, and we evaluate the acute and long-term effects of Brazilian nuts (BN: 15 g of Brazil nuts + 30 g of cashew nuts) included in an energy-restricted intervention on food intake, appetite, and peptide hormones. We conducted an 8-week, randomized, open-label, controlled, parallel-arm clinical trial with 28 women at cardiometabolic risk who received an energy-restricted diet containing BN or an energy-restricted nut-free diet (control). At baseline and after 8 weeks of intervention, subjective postprandial appetite ratings were assessed using a visual analog scale (VAS) before and after consumption (0, 10, 60, 120, 180, and 240 minutes) of a 437-kcal nut-enriched (BN group) or nut-free (control) breakfast meal. Subsequently, an ad libitum lunch was served, and the participants completed another VAS at 280 minutes. Plasma concentrations of ghrelin, glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, and leptin were measured at fasting and postprandially at 60, 120, and 240 minutes. Last, subsequent reported 24-hour energy intake was assessed in a free-living setting. BN consumption did not have acute effects on food intake, appetite, or peptide hormones. However, after an 8-week intervention, postprandial ghrelin (difference between post- and preintervention area under the curve) decreased in the BN group in comparison to the control (mean difference, 1978 pg/mL/min, 95% CI, 27-3929 pg/mL/min; P = .047) and therefore, an energy-restricted diet containing demonstrated potential to decrease hunger in cardiometabolic risk women.
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Doenças Cardiovasculares , Fome , Humanos , Feminino , Grelina , Nozes , Brasil , Dieta , Apetite , Ingestão de Energia , Doenças Cardiovasculares/prevenção & controle , Período Pós-Prandial , Estudos Cross-Over , GlicemiaRESUMO
BACKGROUND: Appetite regulation is integral to food intake and is modulated by complex interactions between internal and external stimuli. Hormonal mechanisms which stimulate or inhibit intake have been characterized, but the physiologic effects of serum levels of such hormones in short-term appetite regulation have received little attention. AIM: To evaluate whether fasting levels of orexigenic/anorexigenic hormones were associated with energy intake at breakfast, served soon after drawing a fasting blood sample, in a group of adolescents. MATERIAL AND METHODS: Anthropometry, body composition and fasting blood levels of leptin, insulin, ghrelin, and orexin-A were measured in 655 Chilean adolescents aged 16.8 ± 0.3 years (52% males). Energy intake was measured at a semi-standardized breakfast. Associations between hormone levels and energy intake were studied using multivariate linear models. RESULTS: Thirty nine percent of participants were overweight/ obese. After an overnight fast, median values for leptin, insulin, ghrelin and orexin-A were 7.3 ng/mL, 6.7 IU/dL, 200.8 pg/mL, and 16.1 pg/mL, respectively. Participants ate on average 637 ± 239 calories at breakfast. In multivariable models, insulin levels were inversely and independently associated with caloric intake at breakfast (β = −18.65; p < 0.05), whereas leptin, ghrelin and orexin-A levels were positively and independently associated with intake: β= 5.56, β = 0.34 and β = 8.40, respectively, p < 0.05. CONCLUSIONS: Fasting leptin, ghrelin and orexin-A were positively associated with energy intake during breakfast provided soon after the blood draw. Insulin was negatively associated with energy intake. Modifiable factors influencing levels of appetite regulating hormones could be a potential target for influencing food intake.
ANTECEDENTES: La regulación del apetito es parte integral de la ingesta alimentaria y es modulada por complejas interacciones entre estímulos internos y externos. Se han caracterizado los mecanismos hormonales que estimulan o inhiben la ingesta, pero los efectos fisiológicos de los niveles séricos de tales hormonas en la regulación del apetito a corto plazo han recibido poca atención. OBJETIVO: Evaluar si los niveles en ayunas de hormonas orexigénicas/ anorexigénicas se asocian con la ingesta energética en el desayuno, entregado inmediatamente después de una muestra de sangre en ayunas, en un grupo de adolescentes. MATERIAL Y MÉTODO: Se efectuaron mediciones antropométricas, composición corporal y medición de niveles en ayunas de leptina, insulina, grelina y orexina-A en 655 adolescentes de 16,8 ± 0,26 años. La ingesta energética se midió en un desayuno semiestandarizado. Se estudiaron las asociaciones entre los niveles hormonales y la ingesta energética mediante modelos lineales multivariados. RESULTADOS: Los valores de leptina, insulina, grelina y orexina-A fueron 7,3 ng/mL, 6,7 UI/dL, 200,8 pg/mL y 16,1 pg/mL respectivamente. Los participantes comieron un promedio de 637 ± 239 calorías en el desayuno. Los niveles de insulina se asociaron inversa e independientemente con la ingesta del desayuno (β = −18,65; p < 0,05), mientras que los niveles de leptina, grelina y orexina-A se asociaron positiva e independientemente con la ingesta: β = 5,65; β = 0,34; β = 8,40, (p < 0,05). CONCLUSIONES: La leptina, grelina y orexina-A en ayunas se asociaron positivamente con la ingesta de energía durante el desayuno proporcionado poco después de la muestra de sangre. La insulina se asoció negativamente con la ingesta de energía. Los factores modificables que influyen en las hormonas reguladoras del apetito podrían ser un objetivo potencial para influir en la ingesta de alimentos.
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Humanos , Masculino , Feminino , Adolescente , Apetite/fisiologia , Desjejum , Ingestão de Energia/fisiologia , Chile , Jejum , Leptina , Grelina , Orexinas , InsulinaRESUMO
Melatonin is a hormone involved in appetite regulation and food intake. Circadian chronorrupture caused by its absence has been associated with excessive food consumption, and there is evidence that exogenous melatonin supplementation can restore homeostasis. Therefore, the aim of this systematic review was to synthesize evidence from randomized controlled clinical and preclinical trials that evaluated the effects of exogenous melatonin supplementation on eating habits and appetite-regulating hormones. The protocol was registered in PROSPERO (number 42020175809). Medline, Scopus, Web of Science and Cochrane Library were systematically searched from January 2020 to February 2021. Of 3.695 articles identified, 2 clinical and 13 preclinical trials (n = 15) met the inclusion criteria. The outcomes were total food intake, calories, macronutrients, cholesterol intake, leptin and ghrelin levels. Interventions ranged from 28 to 336 days and dose of melatonin varied between 0.2 µg/mL of drinking water and 10 mg/day. Clinical trials were conducted with healthy adults, and preclinical trials with rodents and dogs. Of the 15 articles, five assessed food intake and leptin, four assessed food intake only, five assessed leptin only, and one assessed leptin and ghrelin serum levels. The majority of the articles were judged as having low risk of bias. Although findings are heterogeneous and do not allow a robust conclusion, this review adds to the growing body of evidence suggesting that exogenous melatonin may be a potential therapeutic agent against endocrine-metabolic disorders. This reversal is not necessarily associated with changes in food consumption, signaling that melatonin's metabolic effects may occur independently of energy intake. Further studies, especially with humans, are needed provide more evidences for melatonin supplementation in clinical practice, as well as to understand its role on eating habits and appetite-regulating hormones.
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Apetite , Melatonina , Animais , Ritmo Circadiano , Suplementos Nutricionais , Cães , Ingestão de Alimentos , Comportamento Alimentar , GrelinaRESUMO
BACKGROUND: The effect of nonnutritive sweeteners on appetite is controversial. Some studies have found changes in certain appetite control hormones with sucralose intake that may be through interaction with sweet taste receptors located in the intestine. OBJECTIVE: The aim of this study was to evaluate whether sucralose consumption could produce changes in fasting plasma concentrations of appetite-regulating hormones, including glucagon-like peptide 1, ghrelin, peptide tyrosine tyrosine, and leptin, and secondarily in insulin resistance. DESIGN: A 2-week parallel randomized clinical trial with an additional visit conducted 1 week after dosing termination. PARTICIPANTS/SETTING: Sixty healthy, normal-weight individuals, without habitual consumption of nonnutritive sweeteners were recruited from July 2015 to March 2017 in Mexico City. INTERVENTION: Daily sucralose consumption at 15% of the acceptable daily intake by using commercial sachets added to food. The control group followed the same protocol without an intervention. MAIN OUTCOMES MEASURED: Fasting concentrations of appetite regulating hormones before and after the intervention. Fasting glucose and insulin concentrations were measured to assess insulin resistance as a secondary outcome. STATISTICAL ANALYSIS PERFORMED: Basal and final concentrations were compared using Wilcoxon matched-pairs test and Mann-Whitney U test for analysis between groups. Repeated measures analysis of variance was used to evaluate changes in the homeostasis model assessment of insulin resistance. RESULTS: Sucralose was not associated with changes in any of the hormones measured. One week postintervention, an incremental change (P=0.04) in the homeostasis model assessment of insulin resistance was found in the intervention group. CONCLUSIONS: Sucralose intake is not associated with changes in fasting concentrations of glucagon-like peptide 1, ghrelin, peptide tyrosine tyrosine, or leptin. An increase in the homeostasis model assessment of insulin resistance observed only at 1 week postdosing is of unknown clinical significance, if any.
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Dipeptídeos/sangue , Jejum , Grelina/sangue , Peptídeo 1 Semelhante ao Glucagon/sangue , Leptina/sangue , Sacarose/análogos & derivados , Adulto , Apetite/efeitos dos fármacos , Glicemia/análise , Dieta , Feminino , Humanos , Insulina/sangue , Resistência à Insulina , Masculino , México , Sacarose/administração & dosagemRESUMO
The paraventricular nucleus (PVN) is involved in the control of sympathetic tone and the secretion of hormones, both functions known to be influenced by ghrelin, suggesting direct effect of ghrelin in this nucleus. However, the effects of ghrelin on the excitability of different PVN neuronal populations have not been demonstrated. This study assessed the effects of ghrelin on the activity of PVN neurons, correlating the responses to subpopulations of PVN neurons. We used a 64 multielectrode array to examine the effects of ghrelin administration on extracellular spike frequency in PVN neurons recorded in brain slices obtained from male Sprague-Dawley rats. Bath administration of 10 nM ghrelin increased (29/97, 30%) or decreased (37/97, 38%) spike frequency in PVN neurons. The GABAA and glutamate receptors antagonists abolish the decrease in spike frequency, without changes in the proportion of increases in spike frequency (23/53, 43%) induced by ghrelin. The results indicate a direct effect of ghrelin increasing PVN neurons activity and a synaptic dependent effect decreasing PVN neurons activity. The patch clamp recordings showed similar proportions of PVN neurons influenced by 10 nM ghrelin (33/95, 35% depolarized; 29/95, 30% hyperpolarized). Using electrophysiological fingerprints to identify specific subpopulations of PVN neurons we observed that the majority of pre-autonomic neurons (11/18 -61%) were depolarized by ghrelin, while both neuroendocrine (29% depolarizations, 40% hyperpolarizations), and magnocellular neurons (29% depolarizations, 21% hyperpolarizations) showed mixed responses. Finally, to correlate the electrophysiological response and the neurochemical phenotype of PVN neurons, cell cytoplasm was collected after recordings and RT-PCR performed to assess the presence of mRNA for vasopressin, oxytocin, thyrotropin (TRH) and corticotropin (CRH) releasing hormones. The single-cell RT-PCR showed that most TRH-expressing (4/5) and CRH-expressing (3/4) neurons are hyperpolarized in response to ghrelin. In conclusion, ghrelin either directly increases or indirectly decreases the activity of PVN neurons, this suggests that ghrelin acts on inhibitory PVN neurons that, in turn, decrease the activity of TRH-expressing and CRH-expressing neurons in the PVN.
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The study of the factors that regulate high energy food intake is especially relevant nowadays due to the high prevalence of overweight and obesity. Food intake regulation can be divided in two basic processes, namely satiation and satiety. Satiation is the process that determines the moment in which feeding stops and regulates the amount of ingested food during a single meal. Satiety is the interval between meals and regulates the time elapsed between two meals. The longer the interval, the lower energy intake. Each of these processes are regulated by different factors, which are here reviewed.
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Humanos , Regulação do Apetite/fisiologia , Saciação/fisiologia , Ingestão de Energia/fisiologia , Resposta de Saciedade/fisiologia , Sensação/fisiologia , Fatores de Tempo , Ingestão de Alimentos/fisiologiaRESUMO
INTRODUCTION: Obesity, a serious public health problem, occurs mainly when food consumption exceeds energy expenditure. Therefore, energy balance depends on the regulation of the hunger-satiety mechanism, which involves interconnection of the central nervous system and peripheral signals from the adipose tissue, pancreas and gastrointestinal tract, generating responses in short-term food intake and long-term energy balance. Increased body fat alters the gut- and adipose-tissue-derived hormone signaling, which promotes modifications in appetite-regulating hormones, decreasing satiety and increasing hunger senses. With the failure of conventional weight loss interventions (dietary treatment, exercise, drugs and lifestyle modifications), bariatric surgeries are well-accepted tools for the treatment of severe obesity, with long-term and sustained weight loss. Bariatric surgeries may cause weight loss due to restriction/malabsorption of nutrients from the anatomical alteration of the gastrointestinal tract that decreases energy intake, but also by other physiological factors associated with better results of the surgical procedure. OBJECTIVE: This review discusses the neuroendocrine regulation of energy balance, with description of the predominant hormones and peptides involved in the control of energy balance in obesity and all currently available bariatric surgeries. CONCLUSIONS: According to the findings of our review, bariatric surgeries promote effective and sustained weight loss not only by reducing calorie intake, but also by precipitating changes in appetite control, satiation and satiety, and physiological changes in gut-, neuro- and adipose-tissue-derived hormone signaling.
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Cirurgia Bariátrica , Ingestão de Energia , Metabolismo Energético , Hormônios/metabolismo , Sistemas Neurossecretores/metabolismo , Obesidade , Redução de Peso , Tecido Adiposo/metabolismo , Regulação do Apetite , Trato Gastrointestinal/metabolismo , Humanos , Obesidade/etiologia , Obesidade/metabolismo , Obesidade/cirurgia , Peptídeos/metabolismo , SaciaçãoRESUMO
The prevalence of obesity increases worldwide. Treating obesity and its associated health problems has a significant economic impact on health care systems. The unsatisfactory long-term outcomes observed in the obesity treatment are due to its complex pathophysiology and the inherent difficulties associated with maintenance of lifestyle modifications. Determined by genetic and environmental factors, obesity has been officially recognized as a chronic disease, an action that allowed the recognition of anti-obesity drugs as legitimate therapeutic options to address the growing obesity endemic. Like other chronic diseases, obesity requires long-term treatment. Pharmacological interventions, when used as an adjunct to lifestyle changes, are useful to facilitate clinically meaningful weight loss, which may impact on obesity-associated comorbid conditions. In the past, medications for weight reduction were limited. However, the landscape has changed and new drugs provide additional options for weight management. Among the new drugs, liraglutide is the most studied, especially regarding its effects on the limbic system. As an adjunct to a reduced-calorie diet and increased physical activity, treatment with liraglutide 3.0 mg provides a statistically significant and clinically meaningful weight loss. Liraglutide is a glucagon-like peptide 1 (GLP-1) receptor agonist that shares 97% homology to native GLP-1. Receptor agonists of GLP-1, including liraglutide, have emerged as effective therapies for type 2 diabetes and obesity. This review will address the major findings concerning the central regulation of appetite and the main studies that evaluated new drugs for obesity treatment, with a greater focus on liraglutide 3.0 mg.
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A high-fat diet is the main environmental cue that has been studied in the hypothalamus since the discovery of its connection with hypothalamic inflammation. Current evidence shows hypothalamic inflammation as a likely mechanism for the dysregulation on the homeostatic control of energy balance, which leads to metabolic alterations and obesity. Although this mechanism seems to be reversible when set during adulthood, we argue whether dietary fatty acids, during critical periods of development, could affect hypothalamic function permanently and set an increased susceptibility to obesity. We found few experimental studies that looked at programming induced by different fatty acids on the hypothalamus. They clearly showed a connection between maternal fat diet, hypothalamic inflammation and metabolic alterations in the offspring. We found that not only a high-fat diet but also a normolipidic diet with unbalanced quantities of different fatty acids produced diverse inflammatory responses on the hypothalamus. Therefore, strategies of manipulating dietary fatty acids in pregnant and lactating women may have great impact on the population's future health. However, more research is still needed on the effects of fatty acids and the hypothalamic inflammation on programming.
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Encefalite/etiologia , Epigênese Genética/efeitos dos fármacos , Ácidos Graxos/efeitos adversos , Ácidos Graxos/metabolismo , Hipotálamo/efeitos dos fármacos , Animais , Gorduras na Dieta/farmacologia , Metabolismo Energético/efeitos dos fármacos , Ácidos Graxos/farmacologia , Feminino , Humanos , Hipotálamo/metabolismo , GravidezRESUMO
ABSTRACT Body weight is regulated by the ability of hypothalamic neurons to orchestrate behavioral, endocrine and autonomic responses via afferent and efferent pathways to the brainstem and the periphery. Weight maintenance requires a balance between energy intake and energy expenditure. Although several components that participate in energy homeostasis have been identified, there is a need to know in more detail their actions as well as their interactions with environmental and psychosocial factors in the development of human obesity. In this review, we examine the role of systemic mediators such as leptin, ghrelin and insulin, which act in the central nervous system by activating or inhibiting neuropeptide Y, Agouti-related peptide protein, melanocortin, transcript related to cocaine and amphetamine, and others. As a result, modifications in energy homeostasis occur through regulation of appetite and energy expenditure. We also examine compensatory changes in the circulating levels of several peripheral hormones after diet-induced weight loss.
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Humanos , Peso Corporal/fisiologia , Ingestão de Energia/fisiologia , Metabolismo Energético/fisiologia , Tecido Adiposo/metabolismo , Ilustração Médica , Obesidade/etiologia , Obesidade/metabolismoRESUMO
Sleep has a fundamental role in the regulation of energy balance, and it is an essential and natural process whose precise impacts on health and disease have not yet been fully elucidated. The aim of this study was to assess the consequences of different periods of paradoxical sleep deprivation (PSD) and recovery from PSD on lipid profile, oral glucose tolerance test (OGTT) results, and changes in insulin, corticosterone, ghrelin, and leptin concentrations. Three-month-old male Wistar rats weighing 250-350 g were submitted to 24, 96, or 192 h of PSD or 192 h of PSD with 480 h of recovery. The PSD was induced by the multiple platforms method. Subsequently, the animals were submitted to an OGTT. One day later, the animals were killed and the levels of triglycerides, total cholesterol, lipoproteins (low-density lipoprotein, very-low-density lipoprotein, and high-density lipoprotein), insulin, ghrelin, leptin, and corticosterone in plasma were quantified. There was a progressive decrease in body weight with increasing duration of PSD. The PSD induced basal hypoglycemia over all time periods evaluated. Evaluation of areas under the curve revealed progressive hypoglycemia only after 96 and 192 h of PSD. There was an increase in corticosterone levels after 192 h of PSD. We conclude that PSD induces alterations in metabolism that are reversed after a recovery period of 20 days.
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Regulação do Apetite , Glicemia/metabolismo , Hormônios/sangue , Lipídeos/sangue , Privação do Sono/sangue , Privação do Sono/fisiopatologia , Sono , Animais , Biomarcadores , Peso Corporal , Corticosterona/sangue , Modelos Animais de Doenças , Ingestão de Alimentos , Metabolismo Energético , Grelina/sangue , Teste de Tolerância a Glucose , Insulina/sangue , Leptina/sangue , Masculino , Ratos Wistar , Recuperação de Função Fisiológica , Fatores de TempoRESUMO
Obese women with polycystic ovary syndrome (PCOS) may have impairment in the regulation of food intake associated with ghrelin and insulin. In order to compare postprandial ghrelin and insulin responses to an ad libitum meal, we assessed 30 obese women with PCOS and 23 obese women without PCOS (control group). Blood samples were taken under fasting conditions, preprandially, and 15, 45, 75, and 135 minutes after the beginning of an ad libitum meal and ghrelin and insulin concentrations were analyzed. Insulin resistance (IR) was classified using basal insulin, quantitative insulin sensitivity check index, and homeostasis model assessment index. Mean ad libitum food intake was similar between the groups (468 ± 150 vs 444 ± 165 g, P = .60). The IR was found in 56.6% in PCOS group compared with 30.4% in the control group (P < .01). The postprandial ghrelin response was similar in both the groups but the insulin area under the curve (AUC) tend to be greater in the PCOS group (12807 ± 8149.4 vs 8654.4 ± 7232.3 µIU/mL/min; P = .057). The ghrelin AUC was negatively correlated with the insulin AUC (r = -.5138; P = .01) only in the control group. The imbalance in the feedback mechanisms between insulin and ghrelin, present in obese women, especially those with IR, may affect food intake throughout the day and that could be a mechanism for the development of obesity in PCOS.
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Este trabalho revisa a participação do sistema serotonérgico no controle da ingestão de alimentos e saciedade. É de grande interesse compreender a relevância desse sistema para o controle fisiológico do balanço energético e da obesidade. Mais de 35 anos de pesquisas sugerem que a serotonina (5-HT) desempenha um importante papel na saciedade. Assim, o sistema serotonérgico tem sido um alvo viável para o controle de peso. A 5-HT apresenta controle sobre a fome e a saciedade através de diversos receptores, com diferentes funções. O receptor 5-HT2C parece ser o mais importante na relação entre ingestão alimentar e balanço energético. Nesta revisão serão discutidos os mecanismos do sistema serotonérgico envolvidos no controle da ingestão de alimentos e saciedade.
This paper reviews involvement of the serotonergic system in the control of food intake and satiety. It is of great interest to understand the relevance of this system for physiological control of energy balance and obesity. Over 35 years of research suggest that serotonin (5-HT) plays an important role in satiety. Thus, the serotonergic system has been a viable target for weight control. The 5-HT has control over hunger and satiety through different receptors with distinct functions. The 5-HT2C receptor may be more important in the relationship between food intake and energy balance. This review will discuss the mechanisms of the serotonergic system involved in the control of food intake and satiety.