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Peripheral glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK) are secreted from enteroendocrine cells, and their plasma concentrations increase in response to eating. While the satiating effect of gut-derived CCK on food intake control is well documented, the effect of peripheral GLP-1 is less clear. There is evidence that native GLP-1 can inhibit food intake only in the fed state but not in the fasting state. We therefore hypothesised that other gut peptides released during a meal might influence the subsequent effect of endogenous GLP-1 and investigated whether CCK could do so. We found that intraperitoneal injection of CCK in food-restricted mice inhibited food intake during the first 30 min segment of a one-hour session of ad libitum chow intake and that mice compensated by increasing their intake during the second half of the session. Importantly, this compensatory behaviour was abolished by an intraperitoneal injection of GLP-1 administered following an intraperitoneal injection of CCK and prior to the one-hour session. In vivo activation of the FFA1 receptor with orally administered TAK875 increased plasma CCK concentration and, consistent with the effect of exogenous CCK, we found that prior oral administration of TAK875 increased the eating inhibitory effect of peripherally administered GLP-1. To examine the role of the vagus nerve in this effect, we utilised a saporin-based lesioning procedure to selectively ablate the CCK receptor-expressing gastrointestinal vagal afferent neurones (VANs). We found that the combined anorectic effect of TAK875 and GLP-1 was significantly attenuated in the absence of CCK receptor expressing VANs. Taken together, our results indicate that endogenous CCK interacts with GLP-1 to promote satiation and that activation of the FFA1 receptor can initiate this interaction by stimulating the release of CCK. This article is protected by copyright. All rights reserved.

Recent studies demonstrated that saikosaponin (SS) A and other SSs extracted from Bupleurum falcatum L. (Apiaceae) roots abolished different behaviours motivated by drugs of abuse and palatable foods in rats. The present study was designed to investigate the effect of an SS-enriched extract fraction of B. falcatum roots on operant, oral self-administration of alcohol and chocolate in rats. To this end, female Sardinian alcohol-preferring and Wistar rats were trained to lever-respond for alcohol (15% v/v) and chocolate (5% w/v powdered Nesquik in water), respectively. Acute treatment with B. falcatum extract (0, 0.75, 1.5, and 3 mg/kg, i.p.) reduced, in a dose-related manner, both alcohol and chocolate self-administration. These data confirm the notion that B. falcatum extracts may be a valuable source of pharmacological agents with anti-addictive and anorectic potential. The use of experimental procedures with predictive validity for the human disease adds strength to the translational potential of these results.

Eating behavior is a complex interaction of physiological, psychological, social, and genetic factors that affect the time of eating, the amount of food consumed, and food preferences. Obesity has reached epidemic proportions in the world and it is the leading cause of morbidity and mortality. According to an analysis of 20 prospective studies, the years of life lost due to obesity have now exceeded the years of life lost due to smoking. The epidemic of obesity in the world determines the relevance of research aimed at identifying the factors that contribute to the emergence of this pathological condition. We studied mainly foreign literature on the effect of estrogens on women’s eating behavior and the physiology of adipose tissue. After puberty, women are at greater risk of developing eating disorders than men, possibly due to a more labile psyche. Estrogens contribute to the accumulation of subcutaneous fat, and low estrogen level in menopausal women contributes to an increase in the amount of visceral fat. It is believed that the anorectic effects of estrogens are mediated by the central nervous system, this statement is based on the fact that direct injections of estradiol into the paraventricular nucleus or the arcuate/ventromedial nucleus are most effective for reducing food intake, body weight and increasing motor activity. There is every reason to believe that further clinical, women-focused studies that provide a better understanding of the intracellular signaling pathways responsible for the estrogenic control of food intake will provide new insights into the mechanisms responsible for the greater prevalence of obesity and eating disorders in women.

Obesity is a chronic disease defined by the abnormal or excessive accumulation of fat that causes damage to health, characterized by a body mass index or BMI equal to or above 30. Seduced by the deceptive promise of rapid weight loss and without much effort, people choose to use drugs to lose weight in order to achieve a “perfect body” without effort and without any medical advice, making the indiscriminate use of anorectics. The objective of this study will be to describe the consequences caused by self-medication with anorectic drugs by obese individuals. It is an integrative literature review, a research technique that gathers and synthesizes relevant publications on a delimited topic or issue, in a systematic and orderly way, contributing to the deepening of the knowledge of the investigated topic, making it possible to draw conclusions about an area particular study, with a qualitative nature and temporality with cross-sectional data collection, the method for bibliographic survey consisted of research based on articles on obesity and its treatment, focusing on the adverse factors described in these studies, the search was carried out in the following bases of scientific data: Medline, SciELO, PubMed, Google Scholar, Lilacs. However, society's awareness of the consequences of self-measurement of these drugs must be performed routinely, as well as guidance on the use of these drugs, since the risks of indiscriminate consumption, without medical and pharmaceutical monitoring of anorectics, are many and can lead to various complications for physical health such as tachycardia, high blood pressure, insomnia, irritability. La obesidad es una enfermedad crónica definida por la acumulación anormal o excesiva de grasa que causa daño a la salud, caracterizada por un índice de masa corporal o IMC igual o superior a 30. Seducidas por la engañosa promesa de una pérdida de peso rápida y sin mucho esfuerzo, las personas eligen utilizar fármacos para adelgazar con el fin de conseguir un “cuerpo perfecto” sin esfuerzo y sin ningún consejo médico, haciendo uso indiscriminado de anorexígenos. El objetivo de este estudio será describir las consecuencias que provoca la automedicación con fármacos anoréxicos por parte de individuos obesos. Es una revisión integradora de literatura, técnica de investigación que reúne y sintetiza publicaciones relevantes sobre un tema o cuestión delimitada, de forma sistemática y ordenada, contribuyendo a la profundización del conocimiento del tema investigado, posibilitando extraer conclusiones sobre un área de estudio particular, con carácter cualitativo y temporalidad con recolección de datos de corte transversal, el método para levantamiento bibliográfico consistió en investigaciones basadas en artículos sobre obesidad y su tratamiento, enfocándose en los factores adversos descritos en estos estudios, la búsqueda se realizó en las siguientes bases de datos científicos: Medline, SciELO, PubMed, Google Scholar, Lilacs. Sin embargo, la concienciación de la sociedad sobre las consecuencias de la automedición de estos fármacos debe realizarse de forma rutinaria, así como la orientación sobre el uso de estos fármacos, ya que los riesgos del consumo indiscriminado, sin seguimiento médico y farmacéutico de los anoréxicos, son muchos y pueden acarrear a diversas complicaciones para la salud física como taquicardia, hipertensión arterial, insomnio, irritabilidad. A obesidade é uma doença crônica definida pelo acúmulo anormal ou excessivo de gordura que acarreta prejuízos à saúde, caracterizada pelo índice de massa corporal ou IMC igual ou acima de 30. Seduzidas pela enganosa promessa de emagrecimento rápido e sem muito empenho, as pessoas optam por utilizar medicamentos para emagrecer com intuito de conseguir um “corpo perfeito” sem esforço e sem qualquer orientação médica, realizando o uso indiscriminado de anorexígenos. O objetivo desse estudo consistirá em descrever as consequências causadas pela automedicação com fármacos anorexígenos por indivíduos obesos. Trata-se de uma revisão integrativa de literatura, técnica de pesquisa que reúne e sintetiza publicações relevantes sobre um delimitado tema ou questão, de modo sistêmico e ordenado, contribuindo para o aprofundamento do conhecimento do tema investigado, possibilitando elaborar conclusões a respeito de uma área particular de estudo, com natureza qualitativa e temporalidade com coleta de dados transversal, o método para levantamento bibliográfico consistiu na pesquisa baseada em artigos sobre a obesidade e o tratamento dela, com foco nos fatores adversos descritos nesses estudos, a busca foi realizada nas seguintes bases de dados científicas: Medline, SciELO, PubMed, Google Scholar, Lilacs. Contudo, a conscientização da sociedade quanto às consequências da automedição dessas drogas, deve ser realizada rotineiramente, bem como como realizar a orientação de uso destes fármacos, pois os riscos do consumo indiscriminado, sem acompanhamento médico e farmacêutico dos anorexígenos, são muitos e podem acarretar diversas complicações para a saúde física tais como a taquicardia, a hipertensão arterial, a insônia, a irritabilidade.

The aim of this review is to explore how metabolic changes induced by diets high in saturated fat (HFD) affect nucleus accumbens (NAc) dopamine neurotransmission and food intake, and to explore how stress and inflammation influence this process. Recent evidence linked diet-induced obesity and HFD with reduced dopamine release and reuptake. Altered dopamine neurotransmission could disrupt satiety circuits between NAc dopamine terminals and projections to the hypothalamus. The NAc directs learning and motivated behaviours based on homeostatic needs and psychological states. Therefore, impaired dopaminergic responses to palatable food could contribute to weight gain by disrupting responses to food cues or stress, which impacts type and quantity of food consumed. Specifically, saturated fat promotes neuronal resistance to anorectic hormones and activation of immune cells that release proinflammatory cytokines. Insulin has been shown to regulate dopamine neurotransmission by enhancing satiety, but less is known about effects of diet-induced stress. Therefore, changes to dopamine signalling due to HFD warrant further examination to characterise crosstalk of cytokines with endocrine and neurotransmitter signals. A HFD promotes a proinflammatory environment that may disrupt neuronal endocrine function and dopamine signalling that could be exacerbated by the hypothalamic–pituitary–adrenal and κ-opioid receptor stress systems. Together, these adaptive changes may dysregulate eating by changing NAc dopamine during hedonic versus homeostatic food intake. This could drive palatable food cravings during energy restriction and hinder weight loss. Understanding links between HFD and dopamine neurotransmission will inform treatment strategies for diet-induced obesity and identify molecular candidates for targeted therapeutics.

PURPOSE This study aimed to determine if energy intake and appetite regulation differ in response to an acute bout of resistance exercise (REx) versus aerobic exercise (AEx). METHODS Physically inactive adults (n = 24, 35% ± 2% body fat, 50% female) completed three conditions: AEx (walking at 65%-70% heart rate max for 45 min), REx (1 set to failure of 12 exercises), and sedentary control (SED). Each condition was initiated in the postprandial state (35 min after breakfast). Appetite (visual analog scale for hunger, satiety, and prospective food consumption) and hormones (ghrelin, peptide YY (PYY), and glucagon-like peptide-1 (GLP-1)) were measured before and 30, 90, 120, 150, and 180 min after a standardized breakfast. Area under the curve was calculated using the trapezoid method. Ad libitum energy intake was evaluated at a lunch meal after the 180-min measurements. RESULTS No differences in ad libitum energy intake (REx, 991 ± 68; AEx, 937 ± 65; SED, 944 ± 76 kcal; P = 0.50) or appetite ratings (all, P > 0.05) were detected. The area under the curve for ghrelin, PYY, and GLP-1 were all lower after REx versus AEx (ghrelin: 130,737 ± 4928 for REx; 143,708 ± 7500 for AEx (P = 0.006); PYY: 20,540 ± 1177 for REx, 23,812 ± 1592 for AEx (P = 0.001); and GLP-1: 1314 ± 93 for REx, 1615 ± 110 for AEx (P = 0.013)). Neither exercise condition significantly differed from SED. CONCLUSIONS Acute REx lowers both orexigenic (ghrelin) and anorectic (PYY and GLP-1) gut peptides compared with acute AEx. Ad libitum energy intake did not increase compared with SED in either exercise condition, indicating both exercise modalities have appetite and energy intake suppressing effects. Future work is needed to determine if exercise of differing modalities influences chronic appetite regulation.

There is an on-going debate about medicinal use of kratom plant (Mitragyna speciosa (MS)) on whether it has beneficial or adverse effects. This study aimed to examine long-term weight-reducing effects, toxicity, and dopamine pathway activation of MS alkaloid extract on adult male Wistar rats. In anorexic study, the rats were divided into 3 groups (n = 10), receiving intragastric administration once a day for 19 weeks as control (distilled water), chronic (20 mg/kg MS alkaloid extract) and withdrawal (20 mg/kg MS alkaloid extract for week 1-12 and distilled water for week 13-19) groups. Body weights were measured daily, and blood samples were collected at the end of study for biochemical and hematological tests. In immunohistochemistry, the effects of the extract (40 and 80 mg/kg) on the nucleus accumbens (NAc) and striatum (STr) were determined by using Fos-like immunoreactivity. From week 2 to 19, the results showed a significant reduction in body weight gain produced by the extract. Cessation of the treatment at week 12 did not result in a rebound weight gain. Chronic MS alkaloid extract treatment significantly decreased non-fasting blood sugar, triglyceride, uric acid and blood urea nitrogen (BUN). However, elevated SGOT may suggest possible hepatotoxicity. Chronic MS alkaloid extract treatment also produced baseline levels for most of the hematological parameters except a decrease of monocyte. In immunohistochemistry, the acute treatment did not induce Fos-like immunoreactivity in the NAc and STr. These data demonstrated the beneficial effects of the MS alkaloid extract for possible treatment of metabolic syndromes without toxicity and rewarding effect.

Drug combinations are being studied as potential therapies to increase the efficacy or improve the safety profile of weight loss medications. This study was designed to determine the anorectic interaction and safety profile of 5-hydroxytryptophan (5-HTP)/carbidopa + diethylpropion and 5-HTP/carbidopa + phentermine combinations in rats. The anorectic effect of individual drugs or in combination was evaluated by the sweetened milk test. Isobologram and interaction index were employed to determine the anorectic interaction between 5-HTP/carbidopa and diethylpropion or phentermine. Plasma serotonin (5-HT) was measured by ELISA. Safety of repeated doses of both combinations in rats was evaluated using the tail sphygmomanometer, cardiac ultrasound, hematic biometry and blood chemistry. A single oral 5-HTP, diethylpropion or phentermine dose increased the anorectic effect, in a dose-dependent fashion, in 12 h-fasted rats. A dose of carbidopa at 30 mg/kg reduced the 5-HTP-induced plasmatic serotonin concentration and augmented the 5-HTP-induced anorectic effect. Isobologram and interaction index indicated a potentiation interaction between 5-HTP/30 mg/kg carbidopa + diethylpropion and 5-HTP/30 mg/kg carbidopa + phentermine. Chronic administration of experimental ED40 of 5-HTP/30 mg/kg carbidopa + phentermine, but not 5-HTP/30 mg/kg carbidopa + diethylpropion, increased the mitral valve leaflets area. Moreover, there were no other significant changes in cardiovascular, hematic or blood parameters. Both combinations induced around 20% body weight loss after 3 months of oral administration. Results suggest that 5-HTP/30 mg/kg carbidopa potentiates the anorectic effect of diethylpropion and phentermine with an acceptable safety profile, but further clinical studies are necessary to establish their therapeutic potential in the obesity treatment.

Objetivo: Discutir ações do exercí­cio fí­sico na modulação do apetite e diminuição da ingestão alimentar identificando mecanismos de supressão do apetite e suas ações anorexí­genas. Método: Realizou-se revisão de literatura no Google Scholar, SciELO, Epub e PubMed, utilizando os descritores de pesquisa: obesity, appetite regulation, physical exercise, e anorexigenic para verificar o estado da arte da temática. Foram incluí­das, majoritariamente, publicações em português e inglês, capí­tulos de livros e artigos cientí­ficos. Resultado: O exercí­cio é uma importante ferramenta para prevenção e tratamento da obesidade, sendo uma eficiente ferramenta para redução da gordura corporal, propiciando ação anorexí­gena com supressão do apetite consequentemente diminuição da ingestão alimentar. Conclusão: O efeito de supressão do apetite gerado pela redução dos ní­veis de grelina não é regra, depende de variáveis. A população estudada, ní­vel de condicionamento e intensidade da atividade são determinantes na obtenção dos efeitos de supressão do apetite e diminuição no consumo alimentar.

Introduction: Corticotropin-Releasing Hormone (CRH) is involved in stress and energy homeostasis. On the other hand, CRH receptors also exist within the paraventricular nucleus (PVN) and Central Amygdala (CeA) nuclei. The present study compared the effect of CRH microinjections into PVN and CeA on three consecutive hours and cumulative food intake, internal regulatory factors of food intake, such as serum leptin and ghrelin, as well as blood glucose levels in rats under different acute psychological (Social Stress [SS] and Isolation Stress [IS] group) stresses. Methods: Sixty-six male Wistar rats were randomly allocated to 11 groups: Control, Sham, CRH-PVN, CRH-CeA, SS, IS, SS-CRH-PVN, SS-CRH-CeA, IS-CRH-PVN, and IS-CRH-CeA groups. The CRH (2 µg/kg in 0.5 µL saline) was injected into PVN and CeA nuclei in rats under everyday, acute social stress and isolation stress conditions. Results: Acute isolation and social stresses did not affect cumulative food intake. Whereas isolation stress led to changes in both leptin and glucose levels, social stress reduced only glucose levels. Cumulative food intake significantly decreased under acute CRH injection into the CeA and particularly into the PVN. Blood glucose significantly reduced in all the groups receiving CRH into their CeA. Conclusion: The PVN played a more important role compared to CeA on food intake. These nuclei probably employ different mechanisms for their effects on food intake. Besides, it seems that exogenously CRH injection into the PVN probably had a more anorectic effect than naturally activated CRH by stresses. Acute isolation stress had a greater impact than social stress on leptin level and cumulative food intake. Thus, elevated food intake related to leptin compared to ghrelin and glucose levels in the CRH-PVN group under acute social stress.

The discovery of δ opioid receptor inverse agonist activity induced by ICI-174,864, which was previously reported as an δ opioid receptor antagonist, opened the door for the investigation of inverse agonism/constitutive activity of the receptors. Various peptidic or non-peptidic δ opioid receptor inverse agonists have since been developed. Compared with the reports dealing with in vitro inverse agonist activities of novel compounds or known compounds as antagonists, there have been almost no publications describing the in vivo pharmacological effects induced by a δ opioid receptor inverse agonist. After the observation of anorectic effects with the δ opioid receptor antagonism was discussed in the early 2000s, the short-term memory improving effects and antitussive effects have been very recently reported as possible pharmacological effects induced by a δ opioid receptor inverse agonist. In this review, we will survey the developed δ opioid receptor inverse agonists and summarize the possible in vivo pharmacological effects by δ opioid receptor inverse agonists. Moreover, we will discuss important issues involved in the investigation of the in vivo pharmacological effects produced by a δ opioid receptor inverse agonist.

This study tested the hypothesis whether hypothalamic cocaine-and amphetamine-regulated transcript (CART)-containing systems were involved in photoperiod-induced responses associated with spring migration (hyperphagia and weight gain) and reproduction (gonadal maturation) in migratory songbirds. We specifically chose CART to examine neural mechanism(s) underlying photoperiod-induced responses, since it is a potent anorectic neuropeptide and involved in the regulation of changes in the body mass and reproduction in mammals. We first studied the distribution of CART-immunoreactivity in the hypothalamus of migratory redheaded buntings (Emberiza bruniceps). CART-immunoreactive neurons were found extensively distributed in the preoptic, lateral hypothalamic (LHN), anterior hypothalamic (AN), suprachiasmatic (SCN), paraventricular (PVN), dorsomedialis hypothalami (DMN), inferior hypothalamic (IH), and infundibular (IN) nuclei. Then, we correlated hypothalamic CART-immunoreactivity in buntings with photostimulated seasonal states, particularly winter non-migratory/non-breeding (NMB) state under short days, and spring premigratory/pre-breeding (PMB) and migratory/breeding (MB) states under long days. There were significantly increased CART-immunoreactive cells, and percent fluorescent area of CART-immunoreactivity was significantly increased in all mapped hypothalamic areas, except the SCN, PVN, AN, and DMN in photostimulated PMB and MB states, as compared to the non-stimulated NMB state. In particular, CART was richly expressed in the medial preoptic nucleus, LHN, IH and IN during MB state in which buntings showed reduced food intake and increased night-time activity. These results suggest that changes in the activity of the CART-containing system in different brain regions were associated with heightened energy needs of the photoperiod-induced seasonal responses during spring migration and reproduction in migratory songbirds.

An 8-mo-old male African pygmy hedgehog was anorectic and ataxic; physical examination revealed tetraparesis and a gangrenous left hindlimb. Analgesic and supportive care were administered, but the animal died 3 d after presentation. Postmortem examination revealed a histiocytic sarcoma in a mesenteric lymph node with metastasis to several organs, multifocal vacuolation in the cerebral and cerebellar white matter, and a meningioma in the left lateral ventricle. We diagnosed wobbly hedgehog syndrome (WHS) with disseminated histiocytic sarcoma and lateral ventricular meningioma. Ventricular meningioma, a rare neoplasm in veterinary and human patients, has not been reported previously in hedgehogs, to our knowledge. The neurologic signs in our case were probably caused by the WHS-related vacuolar lesions and are consistent with those of reported WHS cases. Duration of illness was shorter than is typical of WHS cases, which might be related to the disseminated histiocytic sarcoma. Clinical relevance of the lateral ventricular meningioma was not evident because the ventricular mass was localized and not invasive.

Background Glucagon-like peptide-1 receptor agonists (GLP1RA) augment glucose-dependent insulin release and reduce glucagon secretion and gastric emptying, enabling their successful development for the treatment of type 2 diabetes (T2D). These agents also inhibit food intake and reduce body weight, fostering investigation of GLP1RA for the treatment of obesity. Scope of review Here I discuss the physiology of Glucagon-like peptide-1 (GLP-1) action in the control of food intake in animals and humans, highlighting the importance of gut vs. brain-derived GLP-1 for the control of feeding and body weight. The widespread distribution and function of multiple GLP-1 receptor (GLP1R) populations in the central and autonomic nervous system are outlined, and the importance of pathways controlling energy expenditure in preclinical studies vs. reduction of food intake in both animals and humans is highlighted. The relative contributions of vagal afferent pathways vs. GLP1R+ populations in the central nervous system for the physiological reduction of food intake and the anorectic response to GLP1RA are compared and reviewed. Key data enabling the development of two GLP1RA for obesity therapy (liraglutide 3 mg daily and semaglutide 2.4 mg once weekly) are discussed. Finally, emerging data potentially supporting the combination of GLP-1 with additional peptide epitopes in unimolecular multi-agonists, as well as in fixed-dose combination therapies, are highlighted. Major conclusions The actions of GLP-1 to reduce food intake and body weight are highly conserved in obese animals and humans, in both adolescents and adults. The well-defined mechanisms of GLP-1 action through a single G protein-coupled receptor, together with the extensive safety database of GLP1RA in people with T2D, provide reassurance surrounding the long-term use of these agents in people with obesity and multiple co-morbidities. GLP1RA may also be effective in conditions associated with obesity, such as cardiovascular disease and non-alcoholic steatohepatitis (NASH). Progressive improvements in the efficacy of GLP1RA suggest that GLP-1-based therapies may soon rival bariatric surgery as viable options for the treatment of obesity and its complications.

The peptide hormone GDF15 is a potent anorectic factor. Raised circulating levels of GDF15 are seen in a large number of pathological disorders and are associated invariably with adverse clinical outcomes. GDF15 signalling is mediated through GFRAL receptor in the hindbrain. A greater understanding of the mechanisms that drive expression of GDF15 within different tissues has led to the GDF15-GFRAL axis being considered a route through which somatic distress is signalled to the brain. We highlight key recent insights into the role of GDF15 in appetitive behaviour and reflect on the therapeutic potential of the system for disorders of energy balance.

The gastrointestinal tract transmits feeding-regulatory signals to the brain via neuronal and hormonal pathways. Here we studied the interaction between the orexigenic gastric peptide, ghrelin, and the anorectic intestinal peptide, glucagon-like peptide 1 (GLP-1), in terms of feeding regulation via the vagal afferents. GLP-1 preadministration 30 min before ghrelin administration to rats and mice abolished ghrelin-induced food intake, while ghrelin preadministration abolished the anorectic effect of GLP-1. Ghrelin preadministration suppressed GLP-1-induced Fos expression in the nodose ganglia (NG). Electrophysiological assessment confirmed that the initially administered peptide abolished the vagal afferent electrical alteration induced by the subsequently administered peptide. Both the growth hormone secretagogue receptor (GHSR) and the GLP-1 receptor (GLP-1R) are co-localised in a major proportion of NG neurons that innervate the stomach. In these Ghsr+Glp1r+ neurons, ghrelin preadministration abolished the GLP-1-induced calcium response. Ghrelin generated a hyperpolarising current and GLP-1 generated a depolarising current in isolated NG neurons in a patch-clamp experiment. Ghrelin and GLP-1 potently influenced each other in terms of vagally mediated feeding regulation. This peptidergic interaction allows for fine control of the electrophysiological properties of NG neurons.

We previously found that equol, a metabolite of intestinal bacterial conversion from soy isoflavone daidzein, has female-specific anorectic effects. In the present study, we used seven-week-old female ovariectomized (OVX) Sprague Dawley rats to test the hypothesis that the anorectic effect of dietary daidzein may be attributed to delayed gastric emptying. Results suggest that dietary daidzein delays gastric emptying and that it has an anorectic effect with residual gastric contents, but not without gastric contents. Dietary equol significantly decreased daily food intake in the OVX rats without sleeve gastrectomy, but not in those with sleeve gastrectomy, suggesting that the accumulation of food in the stomach is required for the anorectic effect of equol to occur. These results support the hypothesis that the anorectic effect of dietary daidzein is attributed to delayed gastric emptying.

International audience; BackgroundConstitutional thinness (CT), a non‐malnourished underweight state with no eating disorders, is characterized by weight gain resistance to high fat diet. Data issued from muscle biopsies suggested blunted anabolic mechanisms in free‐living state. Weight and metabolic responses to protein caloric supplementation has not been yet explored in CT.MethodsA 2 week overfeeding (additional 600 kcal, 30 g protein, 72 g carbohydrate, and 21 g fat) was performed to compare two groups of CTs (12 women and 11 men) to normal‐weight controls (12 women and 10 men). Bodyweight, food intake, energy expenditure, body composition, nitrogen balance, appetite hormones profiles, and urine metabolome were monitored before and after overfeeding.ResultsBefore overfeeding, positive energy gap was found in both CT genders (309 ± 370 kcal in CT‐F and 332 ± 709 kcal in CT‐M) associated with higher relative protein intake per kilo (1.74 ± 0.32 g/kg/day in CT‐F vs. 1.16 ± 0.23 in C‐F, P < 0.0001; 1.56 ± 0.36 in CT‐M vs. 1.22 ± 0.32 in C‐M, P = 0.03), lower nitrogen (7.26 ± 2.36 g/day in CT‐F vs. 11.41 ± 3.64 in C‐F, P = 0.003; 9.70 ± 3.85 in CT‐M vs. 14.14 ± 4.19 in C‐M, P = 0.02), but higher essential amino acids urinary excretion (CT/C fold change of 1.13 for leucine and 1.14 for arginine) in free‐living conditions. After overfeeding, CTs presented an accentuated positive energy gap, still higher than in controls (675 ± 540 in CTs vs. 379 ± 427 in C, P = 0.04). Increase in lean mass was induced in both controls genders but not in CTs (a trend was noticed in CT women), despite a similar nitrogen balance after overfeeding (5.06 ± 4.33 g/day in CTs vs. 4.28 ± 3.15 in controls, P = 0.49). Higher anorectic gut hormones' tone, glucagon‐like peptide 1 and peptide tyrosine tyrosine, during test meal and higher snacking frequency were noticed before and after overfeeding in CTs.ConclusionsThe blunted muscle energy mechanism, previously described in CTs in free‐living state, is associated with basal saturated protein turn over suggested by the concordance of positive nitrogen balance and an increased urine excretion of several essential amino acids. This saturation cannot be overpassed by increasing this spontaneous high‐protein intake suggesting a resistance to lean mass gain in CT phenotype.

Introduction: Fenfluramine (3‐trifluoromethyl‐N‐ethylamphetamine), a former anorectic agent, has been successfully repurposed for Dravet syndrome (DS).Area covered: A systematic review of data on f...

Objective The aim of this study was to determine whether downstream [peroxisome proliferator-activated-receptor alpha (PPARα) and the G-protein coupled receptor, GPR119] and upstream (a fatty acid translocase, CD36) signaling targets of N-oleoylethanolamide (OEA) were necessary for weight loss, metabolic improvements, and diet preference following vertical sleeve gastrectomy (VSG). Summary background data OEA is an anorectic N-acylethanolamine produced from dietary fats within the intestinal lumen that can modulate lipid metabolism, insulin secretion, and energy expenditure by activating targets such as PPARα and GPR119. Methods Diet-induced obese mice, including wild-type or whole body knockout (KO) of PPARα, GPR119, and CD36, were stratified to either VSG or sham surgery before body weight, body composition, diet preference, and glucose and lipid metabolic endpoints were assessed. Results We found increased duodenal production of OEA and expression of both GPR119 and CD36 were upregulated in wild-type mice after VSG. However, weight loss and glucose tolerance were improved in response to VSG in PPARαKO, GPR119KO, and CD36KO mice. In fact, VSG corrected hepatic triglyceride dysregulation in CD36KO mice, and circulating triglyceride and cholesterol levels in PPARαKO mice. Lastly, we found PPARα-mediated signaling contributes to macronutrient preference independent of VSG, while removal of CD36 signaling blunts the VSG-induced shift toward carbohydrate preference. Conclusions In the search for more effective and less invasive therapies to help reverse the global acceleration of obesity and obesity-related disease OEA is a promising candidate; however, our data indicate that it is not an underlying mechanism of the effectiveness of VSG.

Monoacylglycerol O‐acyltransferase 2 (MGAT2) is one of the key enzymes responsible for triglyceride (TG) re‐synthesis in the small intestine. We have previously demonstrated that pharmacological inhibition of MGAT2 has beneficial effects on obesity and metabolic disorders in mice. Here, we further investigate the effects of MGAT2 inhibition on (a) fat‐induced gut peptide release and fat intake in normal mice and (b) metabolic disorders in high‐fat diet (HFD)‐fed ob/ob mice, a model of severe obesity and type 2 diabetes mellitus, using an orally bioavailable MGAT2 inhibitor Compound B (CpdB). CpdB inhibited elevation of plasma TG in mice challenged with an oil‐supplemented liquid meal. Oil challenge stimulated the secretion of two gut anorectic hormones (peptide tyrosine–tyrosine and glucagon‐like peptide‐1) into the bloodstream, and these responses were augmented in mice pretreated with CpdB. In a two‐choice test using an HFD and a low‐fat diet, CpdB selectively inhibited intake of the HFD in normal mice. Administration of CpdB to HFD‐fed ob/ob mice for 5 weeks suppressed food intake and body weight gain and inhibited elevation of glycated hemoglobin. These results indicate that pharmacological MGAT2 inhibition modulates fat‐induced gut peptide release and fat intake in normal mice and improves obesity and diabetes in HFD‐fed ob/ob mice and thus may have potential for development into a treatment of obesity and its related metabolic diseases., Monoacylglycerol O‐acyltransferase 2 (MGAT2) is responsible for triglyceride re‐synthesis in the small intestine. Here, we investigate the effects of MGAT2 inhibition on (a) fat‐induced gut peptide release and fat intake in normal mice and (b) metabolic disorders in ob/ob mice fed on a high‐fat diet, a model of severe obesity and type 2 diabetes, using a selective MGAT2 inhibitor.

Objective: To investigate the anorexigenic and anti-obesity effectiveness of electroacupuncture (EA) on high-fat-diet-induced (HFDI) obese rats with insulin resistance (IR) and to reveal the possible mechanisms of EA affecting SIRT1 (silent mating type information regulation 2 homolog 1) in the central nervous system (CNS). Methods: We divided 60 rats into 6 groups. All interventions, including EA and intracerebroventricular administration, were performed after 8 weeks of model establishment. We tested obesity phenotypes like body weight (BW) gain; food intake; and IR levels including glucose infusion rate, intraperitoneal insulin tolerance test (IPITT), and intraperitoneal glucose tolerance test (IPGTT) during treatment. We detected protein expression and microscopic locations in hypothalamic SIRT1, the transcription factor FOXO1 (forkhead box protein O1), acetylated FOXO1 (Ac-FOXO1), pro-opiomelanocortin (POMC), and neuropeptide Y (NPY) via Western blotting and immunofluorescence, and monitored gene expression by real-time polymerase chain reaction. Results: Like the SIRT1 agonist, EA suppressed BW gain and IR levels in obese rats, but this was only partially blocked by the SIRT1 antagonist. EA could upregulate protein expression of hypothalamic SIRT1 and downregulate the acetylation level of FOXO1 in the hypothalamic arcuate nucleus (ARC), which decreased gene expression of NPY and increased that of POMC. The agonist targeted the hypothalamic SIRT1 gene, unlike EA, which targeted posttranscriptional regulation. Conclusion: EA could improve obesity in HFDI rats with IR via its anorectic effect. This effect targeted posttranscriptional regulation of the SIRT1 gene, which induced upregulation of ARC FOXO1 deacetylation and mediated the gene expression of POMC and NPY.

Objective Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are effective medications to reduce appetite and body weight. These actions are centrally mediated; however, the neuronal substrates involved are poorly understood. Methods We employed a combination of neuroanatomical, genetic, and behavioral approaches in the mouse to investigate the involvement of caudal brainstem cholecystokinin-expressing neurons in the effect of the GLP-1RA exendin-4. We further confirmed key neuroanatomical findings in the non-human primate brain. Results We found that cholecystokinin-expressing neurons in the caudal brainstem are required for the anorectic and body weight-lowering effects of GLP-1RAs and for the induction of GLP-1RA-induced conditioned taste avoidance. We further show that, while cholecystokinin-expressing neurons are not a direct target for glucose-dependent insulinotropic peptide (GIP), GIP receptor activation results in a reduced recruitment of these GLP-1RA-responsive neurons and a selective reduction of conditioned taste avoidance. Conclusions In addition to disclosing a neuronal population required for the full appetite- and body weight-lowering effect of GLP-1RAs, our data also provide a novel framework for understanding and ameliorating GLP-1RA-induced nausea — a major factor for withdrawal from treatment., Highlights • CCKAP/NTS neurons are required for the full anorectic and body weight-lowering effect of GLP-1 receptor agonists. • GLP-1 receptor agonists promote the formation of conditioned taste avoidance by activating CCKAP/NTS neurons. • CCKAP/NTS neurons are not activated in response to GIP receptor agonists. • GIP receptor agonists reduce GLP-1 receptor agonist-induced neuronal responses in the caudal brainstem. • GIP receptor agonists reduce GLP-1 receptor agonist-induced conditioned taste avoidance.

Anorexia nervosa (AN) has high rates of mortality and low rates of recovery, with outcomes that worsen with illness duration. Improved early intervention strategies are required and identifying risk factors that contribute to the development of AN is critical to their implementation. The development of AN often follows a pre-existing diagnosis of anxiety disorders and obsessive-compulsive disorder and substantial genetic overlap between these conditions suggest common underlying features may predict vulnerability to AN. Moreover, patients with AN have increased levels of circulating proinflammatory cytokines, which may be involved in susceptibility to pathological weight loss considering that children with immune dysfunction have a higher risk of subsequent AN diagnoses.Here, we used the activity-based anorexia (ABA) model to examine whether baseline levels of locomotion, anxiety-like behaviour, compulsive behaviour, and circulating immune markers predict the subsequent development of pathological weight loss in adolescent female rats. While none of these primary features were shown to differentiate rats that went on to be susceptible or resistant to weight loss in ABA, increased locomotion and anxiety-like behaviour were both associated with the extent of weight loss in susceptible but not resistant animals. Intriguingly, behaviour related to poor decision-making in a situation of conflict was shown to predict vulnerability to ABA. Future research using the ABA model to uncover early predictors of AN should focus on translationally relevant assays of decision-making and cognitive behaviour, dysfunction of which may not only predispose animals to ABA but may also represent an endophenotype linking anorectic, anxiety-like and compulsive behaviour.

Although soybean protein is the major component in livestock feeds, its effect on pigs' appetites is largely unknown. Recently, the importance of gut nutrient-sensing for appetite modulation by regulating anorectic gut hormone release has been recognised. This study investigates the roles of soybean proteins in appetite regulation, anorectic gut hormone secretion, and underlying mechanisms. The duodenal-cannulated piglets were used to evaluate the effects of soybean protein hydrolysate (SPH) on feed intake and anorectic hormone release, including cholecystokinin (CCK), peptide YY (PYY), glucagon-like peptide 1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) in the hepatic vein by infusing SPH. Identifying which nutrient-sensing receptor in pig duodenum response to SPH stimulation for gut hormone release was conducted. Using its antagonist, the role of the identified receptor in feed intake and anorectic hormone release was also investigated. Combination with an ex vivo perfusion system, the possible mechanism by which SPH exerts the effects in porcine duodenum was further illustrated. Results in vivo showed that intraduodenal infusion of SPH inhibited short-term feed intake in pigs and promoted CCK, PYY, and GIP secretion in the hepatic vein. SPH also increased duodenum calcium-sensing receptor (CaSR) expression. Pre-treated with CaSR antagonist NPS 2143, the feed intake of pigs tended to be attenuated by SPH (P = 0.09), and CCK release was also suppressed (P < 0.05), indicating that CaSR was involved in SPH-stimulated CCK release and inhibited feed intake in pigs. The ex vivo perfused duodenum tissues revealed that SPH-triggered CCK secretion was likeliest due to the activation of the intracellular Ca2+/TRPM5 pathway. Overall, this study's result illustrates that the diet soybean protein might decrease appetite in pigs by triggering duodenum CCK secretion by activating CaSR and the intracellular Ca2+/TRPM5 pathway.

Obesity is a disease that is currently one of the biggest nutritional problems that can lead to the development of several health injuries. The treatment of the disease consists in the change of daily and eating habits or, in some cases, using anorectics. These medications, in addition to treating obesity, are also related to factors such as body dissatisfaction and the standards imposed by society about women’s appearance. This study aims to evaluate and understand the main risks and side effects of the use of the anorectics in women in the state of São Paulo. The method for the development of the present article was through scientific articles on platforms such as Scientific Electronic Library Online (SciELO), PubMed, Academic Google and Science Direct, and the use of online questionnaire disclosed through social media, which obtained 217 responses. When evaluated the use of anorectics and their conditions of use, it was noticed that the most sought drug was sibutramine with 41,94%. It was also observed that there was a low adherence to the pharmacological treatment associated to physical activity and dietary changes. Most interviewed women presented side effects such as nauseas, headache, diarrhoea, mood swings and dry mouth. And 47,50% of the participants did not received professional monitoring, which demonstrates the lack of knowledge regarding the risks of anorectic drugs, since 23,04% see it as a way of quick weight loss. La obesidad es una patología que em la actualidad presenta uno de los mayores problemas nutricionales, que pueden conducir al desarollo de varias lesiones a la salud. El tratamiento de esta consiste en cambiar los hábitos alimeticos y diarios, en algunos casos, utilizar medicamento anorexígenos. Estas drogas, además de tratar la obesidade, también están relacionados con factores como la insatisfacción corporal, y los estándares impuestos por la sociedad sobre la apariencia de las mujeres. El estudio tiene como objetivo evaluar y comprender los principales riesgos y efectos colaterales del uso dos anorexígenos en mujeres del Estado de São Paulo. El método para el desarrollo del presente artículo fue a través de artículos científicos en plataformas como Scientific Eletronic Library Online (SciELO), PubMed, Google Acadêmico y Science Direct, además de utilización de un cuestionario online que se difunde en las redes sociales, el cual obtuvo 217 respuestas. Al evaluar el uso de anorexígenos y sus condiciones de uso, se notó que el fármaco más buscado fue la sibutramina con 41,94%. También se observo uma baja adherencia en la asociación del tratamiento farmacológico con la actividad física y los cambios dietéticos. La mayoría de las mujeres entrevistadas presentaron efectos adversos como náuseas, dolor de cabeza, diarrea, cambios de humor y boca seca. Y el 47,50% de las participantes no recibió seguimiento profesional, lo que demuestra el desconocimiento sobre los riesgos de los anorexígenos, ya que el 23,04% lo ve como una forma de pérdida de peso rápida. A obesidade é uma patologia que atualmente apresenta um dos maiores problemas nutricionais podendo acarretar no desenvolvimento de diversas injurias à saúde. O tratamento desta consiste na mudança de hábitos diários e alimentares ou, em alguns casos, no uso de medicamentos anorexígenos. Esses medicamentos, além do tratamento da obesidade, também estão relacionados a fatores como a insatisfação corporal e dos padrões impostos pela sociedade sobre a aparência das mulheres. O estudo tem como objetivo avaliar e compreender os principais riscos e efeitos colaterais do uso dos anorexígenos em mulheres no estado de São Paulo. O método para o desenvolvimento do presente artigo deu-se através de artigos científicos em plataformas como Scientific Electronic Library Online (SciELO), PubMed, Google Acadêmico e Science Direct, além da utilização de questionário online sendo divulgado pelas mídias sociais que obteve 217 respostas. Ao ser avaliada a utilização dos anorexígenos e suas condições de uso percebeu-se que o medicamento mais procurado foi a sibutramina com 41,94%. Foi também observado uma baixa adesão da associação do tratamento farmacológico com atividades físicas e mudanças alimentícias. A maioria das mulheres entrevistadas apresentaram efeitos adversos, tais como náuseas, dor de cabeça, diarreia, mudanças de humor e boca seca. E 47,50% das participantes não obtiveram acompanhamento profissional, o que demonstra a falta de conhecimento perante aos riscos dos anorexígenos, uma vez que 23,04% veem como uma forma de emagrecimento rápido.

Growth differentiation factor 15 (GDF15) is a stress-induced cytokine that modulates food intake and energy metabolism. Until now, most mechanistic studies on GDF15 rely on pharmacological interventions using exogenous GDF15, but little is known about its mode of action when induced both chronically and endogenously. Mitochondrial stress is one of the most described physiological conditions that induces GDF151, and therefore an important model to study the underlying mechanisms of endogenous GDF15’s action. Here, using a mouse model of mitochondrial dysfunction via elevated respiratory uncoupling in skeletal muscle, we show a circadian oscillation of muscle-derived GDF15 to promote a daytime-restricted anorexia without signs of nausea or reduced physical activity, contrary to findings using recombinant GDF152–5. We find that mitochondrial stress-induced GDF15 associates with increased anxiety and hypothalamic corticotropin releasing hormone (CRH) induction, without further activation of the hypothalamic-pituitary-adrenal (HPA) axis and corticosterone response. Strikingly, the daytime-restricted anorexia, lean phenotype, systemic shift in substrate metabolism and anxiety-like behavior are completely abolished in conditions of mitochondrial stress coupled with genetic ablation of the GDF15 receptor GDNF receptor alpha-like (GFRAL), which is predominantly expressed in the hindbrain. Finally, we demonstrate that stress-induced GDF15-GFRAL signaling is required for hypothalamic CRH induction to control diurnal food intake in a CRH-receptor 1 (CRHR1)-dependent manner. With this, we uncover for the first time a molecular target of the GDF15-GFRAL axis that links anxiolytic and anorectic behavior as downstream effects of the chronic activation of this pathway by mitochondrial stress.

Ghrelin is a stomach-derived peptide hormone with salient roles in the regulation of energy balance and metabolism. Notably, ghrelin is recognized as the most powerful known circulating orexigenic hormone. Here, we systematically investigated the effects of ghrelin on energy homeostasis and found that ghrelin primarily induces a biphasic effect on food intake that has indirect consequences on energy expenditure and nutrient partitioning. We also found that ghrelin-induced biphasic effect on food intake requires the integrity of Agouti-related peptide/neuropeptide Y-producing neurons of the hypothalamic arcuate nucleus, which seem to display a long-lasting activation after a single systemic injection of ghrelin. Finally, we found that different autonomic, hormonal and metabolic satiation signals transiently counteract ghrelin-induced food intake. Based on our observations, we propose a heuristic model to describe how the orexigenic effect of ghrelin and the anorectic food intake-induced rebound sculpt a timely constrain feeding response to ghrelin., Instituto Multidisciplinario de Biología Celular

Objective: Body image disturbances and the attendant negative emotions are two of the major clinical symptoms of eating disorders. The objective of the present experimental study was to shed more light on the degree of association or dissociation between the physiological and emotional response to mirror exposure in patients with restrictive mental anorexia, and on the relationships between the physiological response and characteristics connected with emotional processing.Materials and Methods: Thirty adolescent girls with the restrictive type of anorexia and thirty matched healthy controls underwent bilateral measurement of skin conductance (SC) during rest, neutral stimulus exposure, and mirror exposure, and completed a set of measures focused on emotion regulation competencies, affectivity, and eating disorder pathology.Results: Compared to healthy controls, girls with restrictive anorexia rated mirror exposure as a subjectively more distressful experience. Differences in skin conductance response (SCR) were not significant; however, variance in SCR was substantially greater in the group of anorexia patients as compared to healthy controls. The overall skin conductance level (SCL) was lower in anorexia patients. Increase in SCR during mirror exposure, as opposed to exposure to neutral stimuli, was positively related to the tendency to experience negative emotions, interoceptive sensitivity, body dissatisfaction and suppression, but not to other symptoms of eating pathology or emotional awareness. A post hoc analysis suggested that physiological reactivity might be associated with interoceptive sensitivity to mirror exposure especially in anorectic patients.Conclusion: The study seems to demonstrate some degree of dissociation between psychophysiological reactivity and subjective response to body exposure in patients with restrictive anorexia. Factors affecting differences in psychophysiological responsiveness to body exposure in anorectic patients require further exploration.

Attentional biases to food-related stimuli have been demonstrated in response to hunger as well as during restrained eating. Such biases are often associated with obesity, but healthy-weight individuals who do not self-report hunger have also demonstrated attentional biases to stimuli signalling food using laboratory-based cognitive tasks. Levels of the anorectic neuropeptide oxytocin are elevated by food intake and, when administered intranasally, oxytocin inhibits food intake in the laboratory. To investigate whether oxytocin can affect appetite via an action on attentional processes, 40 adults (29 women; mean age 24.0 years old) self-administered 24 IU of oxytocin or placebo intranasally. Forty minutes after administration, participants ate a small snack to maintain alertness and ameliorate deprivation-induced hunger before starting a computerized dot-probe attentional bias task that presented 180 trials of paired visual stimuli comprising neutral, food, social and/or romantic images (500 ms presentation time). Reaction times to probe stimuli that appeared after the offset of the visual images indicated a significant attentional bias to food pictures after placebo; this effect was significantly attenuated by oxytocin, p < .001. The effect of oxytocin on attentional bias to the food pictures was not altered by the type of stimulus paired with the food image, and was independent of BMI, age, sex, self-rated eating behaviour, and self-reported parental bonding; however, the effect was modulated by self-reported food cravings and trait stress. The findings support and extend previous work which has suggested that oxytocin can counteract attentional biases to food-related stimuli in a sample with anorexia by demonstrating the same effect for the first time in a cohort who do not have an eating disorder.

Sensing of amino acids in fish brain, especially branched-chain amino acids (BCAA) like leucine, is involved in regulation of feed intake through different mechanisms. However, there is limited information regarding the possible involvement of mechanisms dependent on amino acid carriers of the solute carrier families (SLC) known to be key regulators of intracellular leucine concentration, namely L-type amino acid transporter 1 (LAT1), and sodium-dependent neutral amino acid transporter 2 (SNAT2) and 9,(SNAT9), for which evidence of their participation is available in mammals. Comparative analysis amongst sequences revealed a complex pattern of paralogues in Atlantic salmon, for LAT1 (slc7a5aa, slc7a5ab, slc7a5ba, slc7a5bb, slc7a5ca, and slc7a5cb), SNAT2 (slc38a2a and slc38a2b) and SNAT9 (slc38a9). After establishing phylogenetic relationships of the different paralogues evaluated, samples of the selected brain areas were taken from Atlantic salmon to assess tissue distribution of transcripts. In an additional experiment, fish were fed two diets with different levels of leucine (high leucine: 35 g/kg vs. control leucine: 27.3 g/kg). The high leucine diet resulted in lower feed intake and increased mRNA abundance of specific paralogues of LAT1 (slc7a5aa, slc7a5ab, and slc7a5bb) and SNAT2 (slc38a2a and slc38a2b) though apparently not for SNAT9 in brain areas like hypothalamus and telencephalon involved in food intake regulation. The results obtained suggest a role for members of the SLC family in the anorectic effect of leucine and thus their involvement as additional amino acid sensing mechanism not characterised so far in fish regulation of feed intake.

Deoxynivalenol (DON), also known as vomitoxin, is a mycotoxin that can cause antifeeding and vomiting in animals. However, the mechanism of DON inducing anorexia is complicated. Studies have shown that intestinal hormones play a significant part in the anorexia caused by DON. We adopted the “modeling of acute antifeeding in mice” as the basic experimental model, and used two methods of gavage and intraperitoneal injection to explore the effect of intestinal hormones on the antifeedant response induced by DON in mice. We found that 1 and 2.5 mg/kg·bw of DON can acutely induce anorexia and increase the plasma intestinal hormones CCK, PYY, GIP, and GLP-1 in mice within 3 h. Direct injection of exogenous intestinal hormones CCK, PYY, GIP, and GLP-1 can trigger anorexia behavior in mice. Furthermore, the PYY receptor antagonist JNJ-31020028, GLP-1 receptor antagonist Exendin(9-39), CCK receptor antagonist Proglumide, GIP receptor antagonist GIP(3-30)NH2 attenuated both intestinal hormone and DON-induced anorectic responses. These results indicate that intestinal hormones play a critical role in the anorexia response induced by DON.

Purpose Resistant dextrin (RD) supplementation has been shown to alter satiety, glycaemia, and body weight, in overweight Chinese men; however, there are limited data on its effects in other demographic groups. Here, we investigated the effects of RD on satiety in healthy adults living in the United Kingdom. Methods 20 normal weight and 16 overweight adults completed this randomised controlled cross-over study. Either RD (14 g/day NUTRIOSE® FB06) or maltodextrin control was consumed in mid-morning and mid-afternoon preload beverages over a 28-day treatment period with crossover after a 28-day washout. During 10-h study visits (on days 1, 14, and 28 of each treatment period), satietogenic, glycaemic and anorectic hormonal responses to provided meals were assessed. Results Chronic supplementation with RD was associated with higher fasted satiety scores at day 14 (P = 0.006) and day 28 (P = 0.040), compared to control. RD also increased satiety after the mid-morning intervention drink, but it was associated with a reduction in post-meal satiety following both the lunch and evening meals (P P P = 0.035) and 28 (P = 0.030), compared to day 1, following RD supplementation in the normal weight group. Energy intake and anthropometrics were unaffected. Conclusions RD supplementation modified satiety and glycaemic responses in this cohort, further studies are required to determine longer-term effects on body weight control and metabolic markers. Clinicaltrials.gov registration NCT02041975 (22/01/2014)

Abuse of methamphetamine (METH), an illicit psychostimulant, is a growing public health issue. METH abuse during pregnancy is on the rise due to its stimulant, anorectic, and hallucinogenic properties. METH can lead to multiple organ toxicity in adults, including neurotoxicity, cardiovascular toxicity, and hepatotoxicity. It can also cross the placental barrier and have long-lasting effects on the fetus. This review summarizes neurotoxicity, cardiovascular toxicity, hepatotoxicity, toxicity in other organs, and biomonitoring of prenatal METH exposure, as well as the possible emergence of sensitization associated with METH. We proposed the importance of gut microbiota in studying prenatal METH exposure. There is rising evidence of the adverse effects of METH exposure during pregnancy, which are of significant concern.

Overweight and obesity are pathologies that increase dramatically, they are most often associated with diseases such as hypertension, heart failure, stroke, type II diabetes, insulin resistance, dyslipidemias, certain cancers etc .The objective was to conduct an ethnobotanical survey of 4 plants consumed during periods of hunger and to determine the effect of the extracts of these plants on weight gain and food intake.The survey was based on direct dialogue using the respondent's choice language and the use of a questionnaire. Acute toxicity was determined on NMRI mice by orally administering of single dose of 2000 mg/kg. The slimming and anorectic potential of plant extracts was to evaluate the effect of plant extracts on weight gain and food intake of animals treated at 50, 100 and 500 mg/kg. 55 person with an age between 40 and 81 years old were interviewed.Raphionacme daroniigave the highest frequency of citation with 25.42%. All plant species showed no toxicity at 2000 mg/kg.Gardenia erubescensat 50 mg/kg gave a good activity on weight gain with a reduction of 5.18% against the control with an increase of 11.02%.Gardenia erubescensat 500 mg/kg gave the best anorectic activity on the treated animals.These plant extracts are an asset in the search for a new natural and less toxic molecule for the fight against obesity.

Objective Amphetamine was formerly used as a treatment to combat obesity, but amphetamine's use as an appetite suppressant was discontinued because of its significant abuse potential. Most of the rewarding and reinforcing effects of amphetamine differ by sex, with females showing higher levels of drug intake and amphetamine-induced motivation, relapse, and locomotion, but it is unknown whether amphetamine's effects on feeding also differ by sex. Furthermore, previous research on the anorectic effects of amphetamine has been focused primarily on its effects on baseline homeostatic feeding, but it is unknown whether amphetamine also affects hedonic, reward-related feeding, which is an important factor driving the rise in obesity levels. Methods This study tested whether amphetamine alters food intake in a sex-dependent manner in two reward-related feeding paradigms: a sucrose two-bottle choice test and a high-fat/high-sugar binge intake model. Results Amphetamine altered food intake equally in males and females in both paradigms, with higher doses significantly inhibiting feeding and low doses of amphetamine increasing feeding at later time points. Conclusions Amphetamine's effects on feeding and drug reward may be mediated by distinct mechanisms, which could allow for the development of new approaches to combat obesity with limited abuse and addiction-related side effects.

Repetitive physical activity is a well-established intervention to reduce obesity and to prevent weight regain. Besides increased energy expenditure, reduced caloric intake may contribute to exercise-induced weight loss in obesity. Using adipocyte-specific glycoprotein 130 knockout (gp130Δadipo) mice, we recently unravelled that obesity-induced interleukin-6 (IL-6) signalling in adipose tissue contributes to circulating levels of the two anorectic hormones leptin and insulin. Herein, we aimed to investigate the role of adipocyte-specific IL-6 signalling in exercise-mediated appetite control and, hence, weight reduction in obesity. gp130Δadipo and control littermate mice (gp130F/F) were repetitively exercised during a 12-week period of HFD-feeding. Thermogenesis was determined using thermography and food intake as well as energy expenditure were assessed in metabolic cages. Circulating IL-6, insulin and leptin levels were measured using immunoassays. Protein levels of phosphorylated STAT3, JAK2 and Akt were determined in the hypothalamus by Western blot technique. Repetitive physical activity reduced food intake and HFD-induced weight gain in gp130F/F but not gp130Δadipo mice. In contrast, energy expenditure was not different between the genotypes. Circulating insulin and leptin levels were significantly reduced in gp130Δadipo mice. Moreover, hypothalamic leptin and insulin signalling were enhanced in exercised gp130F/F but not gp130Δadipo mice as demonstrated by elevated pSTAT3, pJAK2 and pAkt protein levels. Adipocyte-specific IL-6 signalling is involved in exercise-mediated regulation of food intake and weight reduction in HFD-fed mice.

Ageing is associated with reduced appetite and energy intakes. However, the mechanisms underlying this phenomenon are not fully understood. This systematic review and meta-analysis quantified differences in circulating concentrations of appetite-related hormones between healthy older and younger adults. Six databases were searched through 12th June 2018 for studies that compared appetite-related hormone concentrations between older and younger adults. Data were pooled using random-effects meta-analysis and are presented as standardised mean difference (Hedges’ g) with 95% confidence intervals (95% CI). Thirty-five studies were included involving 710 older adults (mean ± SD; age: 73 ± 5 years) and 713 younger adults (age: 28 ± 7 years). Compared with younger adults, older adults exhibited higher fasted and postprandial concentrations of the anorectic hormones cholecystokinin (Fasted: SMD 0.41 (95% CI 0.24, 0.57); p

Syndrom Gotowości Anorektycznej (SGA) oznacza uwarunkowany psychologicznie, społecznie i kulturowo zespół objawów, które mogą wskazywać na nieprawidłowości w zakresie realizowania potrzeby pokarmowej oraz stosunku do swojego ciała. W pracy przestawiono zależności pomiędzy stanem odżywienia a występowaniem poszczególnych objawów charakterystycznych SGA. Z analizy wynika, że dziewczęta z BMI ˃50 centyla (zarówno z normowagą jak i nadmierną masą ciała) częściej wprowadzały ograniczenia dietetyczne, odczuwały złość, gdy zjadły zbyt dużo, odczuwały obniżony nastrój i niezadowolenie z siebie, czuły się nieatrakcyjne i chciały poprawić swój wygląd w porównaniu do dziewcząt z pozostałych grup. Profilaktyką w zakresie występowania anoreksji powinny zostać objęte dziewczęta niezależnie od stanu odżywienia, jednak szczególną uwagę należy poświęcić dziewczętom z normowagą w górnej granicy normy oraz z nadwagą lub otyłością. Stwierdzony wśród dziewcząt nieważonych najwyższy odsetek dziewcząt z wysokim poziomem SGA wskazuje, że odmowa udziału w pomiarach antropometrycznych może być jednym z kryteriów świadczących o niewłaściwym stosunku do swojego ciała. Słowa kluczowe: syndrom gotowości anorektycznej, zaburzenia odżywiania, stan odżywienia, adolescencja