Assuntos
Transtornos da Alimentação e da Ingestão de Alimentos , Peptídeos Semelhantes ao Glucagon , Humanos , Peptídeos Semelhantes ao Glucagon/uso terapêutico , Peptídeos Semelhantes ao Glucagon/efeitos adversos , Transtornos da Alimentação e da Ingestão de Alimentos/epidemiologia , Transtornos da Alimentação e da Ingestão de Alimentos/induzido quimicamente , Hipoglicemiantes/efeitos adversos , Hipoglicemiantes/uso terapêutico , Fatores de Risco , FemininoRESUMO
Adolescence is a stage in life characterized by important social, cognitive, and physical changes. Adolescents are vulnerable to various psychosocial disorders, including eating disorders. We aimed to investigate the association between unhealthy habits, sociodemographic characteristics, and the practice of self-induced vomiting or laxative misuse in a representative sample of Brazilian adolescent girls and boys. Data from 102,072 students who participated in the National Adolescent School-based Health Survey were analyzed using the dependent variable: presence or absence of self-induced vomiting and/or laxative misuse; independent variables: consumption of unhealthy and high-calorie food items, age during first sexual intercourse, and the use of tobacco, alcohol, and/or illicit drugs. Associations between exposure and outcome were estimated using Poisson's regression models stratified by sex, and including region, school, age group, and mother's educational history as adjustment variables. Eating ultra-processed foods and age during first sexual intercourse were associated with self-induced vomiting and laxative misuse only for girls; all other variables (consuming unhealthy foods and using legal or illicit substances) were associated with these behaviors for both sexes after applying adjustment variables. Early interventions focusing on changing unhealthy behaviors may prevent development of eating disorders in adolescents. Our findings demonstrate a strong association of many unhealthy habits with laxative misuse and self-induced vomiting practices in Brazilian adolescents.
Assuntos
Comportamento do Adolescente , Comportamento Alimentar , Transtornos da Alimentação e da Ingestão de Alimentos , Hábitos , Laxantes/efeitos adversos , Estudantes , Vômito , Adolescente , Brasil/epidemiologia , Criança , Transtornos da Alimentação e da Ingestão de Alimentos/induzido quimicamente , Transtornos da Alimentação e da Ingestão de Alimentos/epidemiologia , Feminino , Humanos , Laxantes/administração & dosagem , Masculino , Fatores SexuaisRESUMO
Vasoactive intestinal peptide (VIP) and corticotrophin-releasing factor (CRF) are anorexigenic neuropeptides that act in the hypothalamus to regulate food intake. Intracerebroventricular (ICV) microinjection of VIP promotes increased plasma adrenocorticotrophic hormone (ACTH) and corticosterone, indicating that VIP activates hypothalamic-pituitary-adrenal axis. The aim of this study was to evaluate the interaction between VIP and CRF, by verifying the effects of ICV administration of VIP on the activity of neurons and CRF mRNA expression in paraventricular nucleus of hypothalamus (PVN). In addition, it was evaluated the effects of pretreatment with CRF type 1 receptor (CRFR1) antagonist (Antalarmin, ANT) or CRF type 2 receptor (CRFR2) antagonist (Antisauvagine-30, AS30) on VIP-induced changes on food intake and plasma parameters of male rats. Compared to Saline group, VIP increased not only the number of Fos-related antigens (FRA)-immunoreactive neurons in the PVN but also CRF mRNA levels in this nucleus. Both ANT and AS30 treatment attenuated the inhibition of food intake promoted by VIP, ANT showing a more pronounced effect. Both antagonists also attenuated VIP-induced reduction and enhancement of free fatty acids and corticosterone plasma levels, respectively, and only AS30 was able to attenuate the hyperglycemia. These results suggest that CRF is an important mediador of VIP effects on energy balance, and CRFR1 and CRFR2 are involved in these responses.
Assuntos
Hormônio Liberador da Corticotropina/fisiologia , Transtornos da Alimentação e da Ingestão de Alimentos/sangue , Transtornos da Alimentação e da Ingestão de Alimentos/induzido quimicamente , Peptídeo Intestinal Vasoativo/efeitos adversos , Hormônio Adrenocorticotrópico/sangue , Animais , Glicemia/efeitos dos fármacos , Glicemia/metabolismo , Corticosterona/sangue , Hormônio Liberador da Corticotropina/genética , Hormônio Liberador da Corticotropina/metabolismo , Ingestão de Alimentos/efeitos dos fármacos , Ingestão de Alimentos/fisiologia , Ácidos Graxos/sangue , Transtornos da Alimentação e da Ingestão de Alimentos/genética , Sistema Hipotálamo-Hipofisário/efeitos dos fármacos , Sistema Hipotálamo-Hipofisário/metabolismo , Hipotálamo/metabolismo , Masculino , Sistema Hipófise-Suprarrenal/efeitos dos fármacos , Sistema Hipófise-Suprarrenal/metabolismo , Ratos , Ratos Wistar , Peptídeo Intestinal Vasoativo/metabolismoRESUMO
Adrenalectomy-induced hypophagia is associated with increased satiety-related responses, which involve neuronal activation of the nucleus of the solitary tract (NTS). Besides its effects on the pituitary-adrenal axis, corticotrophin-releasing factor (CRF) has been shown to play an important role in feeding behaviour, as it possesses anorexigenic effects. We evaluated feeding-induced CRF mRNA expression in the paraventricular nucleus (PVN) and the effects of pretreatment with CRF(2) receptor antagonist (Antisauvagine-30, AS30) on food intake and activation of NTS neurons in response to feeding in adrenalectomised (ADX) rats. Compared to the sham group, ADX increased CRF mRNA levels in the PVN of fasted animals, which was further augmented by refeeding. AS30 treatment did not affect food intake in the sham and ADX+corticosterone (B) groups; however, it reversed hypophagia in the ADX group. In vehicle-pretreated animals, refeeding increased the number of Fos and Fos/TH-immunoreactive neurons in the NTS in the sham, ADX and ADX+B groups, with the highest number of neurons in the ADX animals. Similarly to its effect on food intake, pretreatment with AS30 in the ADX group also reversed the increased activation of NTS neurons induced by refeeding while having no effect in the sham and ADX+B animals. The present results show that adrenalectomy induces an increase in CRF mRNA expression in the PVN potentiated by feeding and that CRF(2) receptor antagonist abolishes the anorexigenic effect and the increased activation of NTS induced by feeding in the ADX animals. These data indicate that increased activity of PVN CRF neurons modulates brainstem satiety-related responses, contributing to hypophagia after adrenalectomy.
Assuntos
Adrenalectomia , Hormônio Liberador da Corticotropina/fisiologia , Ingestão de Alimentos/genética , Transtornos da Alimentação e da Ingestão de Alimentos/genética , Resposta de Saciedade , Adrenalectomia/reabilitação , Animais , Corticosterona/farmacologia , Hormônio Liberador da Corticotropina/genética , Hormônio Liberador da Corticotropina/metabolismo , Regulação para Baixo/efeitos dos fármacos , Ingestão de Alimentos/efeitos dos fármacos , Ingestão de Alimentos/fisiologia , Transtornos da Alimentação e da Ingestão de Alimentos/induzido quimicamente , Transtornos da Alimentação e da Ingestão de Alimentos/metabolismo , Expressão Gênica/efeitos dos fármacos , Antagonistas de Hormônios/farmacologia , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos , Núcleo Hipotalâmico Paraventricular/metabolismo , Fragmentos de Peptídeos/farmacologia , Ratos , Ratos Wistar , Receptores de Hormônio Liberador da Corticotropina/antagonistas & inibidores , Resposta de Saciedade/efeitos dos fármacos , Resposta de Saciedade/fisiologiaRESUMO
Zolpidem is a hypnotic drug used in sleep disorders. It binds selectively to alpha 1 subunit of the GABA A benzodiazepine receptor. Zolpidem reduces sleep latency, number of arousals and increases the total time of sleep. However, it is considered that it may increase phase 3 of non rapid eye movement sleep, where somnambulism can take place. Our aim is to report 8 cases of sleep related eating disorders associated with the use of this drug. We have evaluated the medical history of 8 patients who had received zolpidem for sleeping disorders and who have presented sleep related eating disorders. Eight patients (6 women, 2 men) aged between 32 to 72 years old, which received 10 mg of zolpidem/night except 1 that received 12.5 mg, were presented. They have referred strange eating behavior compatible to sleep related eating disorder. Symptoms appeared at a mean of 39.8 days after starting the medication. The numbers of nocturnal episodes recorded by the family or by the patient were 1 to 8 episodes of nocturnal eating per night. The morning after, patients found leftovers from the night before which they did not recall to have eaten. The remission was complete after discontinuing zolpidem. Zolpidem may induce sleep related eating disorder in about 1% of patients, although we consider there may be a subdiagnosis of this phenomenon. It will be important to bear in mind and look for this side effect because all the episodes could easily be controlled by withdrawing the drug.
Assuntos
Transtornos da Alimentação e da Ingestão de Alimentos/induzido quimicamente , Agonistas de Receptores de GABA-A/efeitos adversos , Hipnóticos e Sedativos/efeitos adversos , Piridinas/efeitos adversos , Sono/efeitos dos fármacos , Sonambulismo/induzido quimicamente , Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Sono/fisiologia , Transtornos do Sono-Vigília/tratamento farmacológico , Síndrome , ZolpidemRESUMO
El zolpidem es una droga hipnótica utilizada para el tratamiento del insomnio. Disminuye la latencia del sueño, el número total de despertares y aumenta el tiempo total del sueño respetando en general su arquitectura. Se cree que aumenta la fase 3 del sueño lento profundo. Nuestro objetivo es comunicar 8 casos de síndrome de ingesta nocturna relacionado al sueño y conductas automáticas complejas asociadas a sonambulismo como efecto colateral del zolpidem. Se analizaron las historias clínicas de 8 pacientes tratados con zolpidem que referían ingesta nocturna de alimentos con amnesia total o parcial del episodio. Se presentan 6 mujeres y 2 hombres, entre 32 y 72 años (media: 58 años), 7 tratados con zolpidem 10 mg/noche y 1 con zolpidem 12.5 mg/noche de liberación prolongada. El tiempo de exposición previo al desarrollo de eventos fue de 1 a 180 días (media de 39.8). El número de episodios relatados era de 1 a 8/noche (media 2.5) asociado con amnesia. Los episodios desaparecieron por completo en el 100% de los casos al suspender la medicación. El síndrome de ingesta nocturna relacionado al sueño es una parasomnia de sueño lento profundo que consiste en episodios de ingesta de alimento o bebida durante la noche, con amnesia parcial o completa del episodio. El zolpidem podría inducir el síndrome de ingesta nocturna relacionado al sueño en aproximadamente el 1% de pacientes, aunque creemos que es un efecto adverso que está subdiagnosticado. Se resuelve simplemente suspendiendo la medicación.
Zolpidem is a hypnotic drug used in sleep disorders. It binds selectively to alpha 1 subunit of the GABA A benzodiazepine receptor. Zolpidem reduces sleep latency, number of arousals and increases the total time of sleep. However, it is considered that it may increase phase 3 of non rapid eye movement sleep, where somnambulism can take place. Our aim is to report 8 cases of sleep related eating disorders associated with the use of this drug. We have evaluated the medical history of 8 patients who had received zolpidem for sleeping disorders and who have presented sleep related eating disorders. Eight patients (6 women, 2 men) aged between 32 to 72 years old, which received 10 mg of zolpidem/night except 1 that received 12.5 mg, were presented. They have referred strange eating behavior compatible to sleep related eating disorder. Symptoms appeared at a mean of 39.8 days after starting the medication. The numbers of nocturnal episodes recorded by the family or by the patient were 1 to 8 episodes of nocturnal eating per night. The morning after, patients found leftovers from the night before which they did not recall to have eaten. The remission was complete after discontinuing zolpidem. Zolpidem may induce sleep related eating disorder in about 1% of patients, although we consider there may be a subdiagnosis of this phenomenon. It will be important to bear in mind and look for this side effect because all the episodes could easily be controlled by withdrawing the drug.
Assuntos
Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Transtornos da Alimentação e da Ingestão de Alimentos/induzido quimicamente , Agonistas de Receptores de GABA-A/efeitos adversos , Hipnóticos e Sedativos/efeitos adversos , Piridinas/efeitos adversos , Sono/efeitos dos fármacos , Sonambulismo/induzido quimicamente , Síndrome , Transtornos do Sono-Vigília/tratamento farmacológico , Sono/fisiologiaRESUMO
Sulpiride (20 mg/kg/ip for 21 days) induced in female rats a significant body weight increase and hyperphagia. After drug withdrawal a significant hypophagia was observed. It is hypothesised that this hypophagia might be a spontaneous manifestation of D2 dopamine receptors supersensitivity, either in the perifornical region of the lateral hypothalamus or in the pituitary.