A CHILD WITH NARCOLEPSY

Introdução: A Narcolepsia é uma doença crónica caracterizada por ataques de sono, sonolência diurna excessiva e fragmentação do sono noturno. Pode associar-se a cataplexia e a outros fenómenos do sono REM (paralisia do sono e alucinações hipnagógicas e hipnopômpicas). Caso clínico: Um menino de 10 anos foi enviado à consulta de Pedopsiquiatria por alterações do comportamento, irritabilidade, adormecimento fácil e distração, sendo interpretado como uma “criança mal-educada”. Após avaliação clínica e estudo concluiu-se que apresentava narcolepsia com cataplexia. Discussão/conclusão: Os doente com narcolepsia confrontam-se com vários problemas devido à própria doença que, se não tratada ou tratada ineficazmente, provoca sintomas perturbadores ou embaraçosos, influenciando a sua qualidade de vida. O objetivo deste trabalho é chamar a atenção para este problema uma vez que é uma situação rara e por isso também muitas vezes desconhecida pelo público em geral e até pelos profissionais de saúde.Introduction: Narcolepsy is a chronic disease characterized by sleep attacks, excessive daytime sleepiness and nocturnal sleep fragmentation. It can be associated cataplexy and other disturbance of REM sleep (sleep paralysis and hypnagogic hallucinations and hypnopompic). Case report: A 10-year old boy was referred to Pedopsychiatry because of behavioural disturbance, irritability, sleepiness and distraction, being interpreted as an “ill-mannered child.” After clinical evaluation and comprehensive laboratory studies we concluded that he presented narcolepsy with cataplexy. Discussion/conclusion: Patients with narcolepsy face several problems due to the disease which, if left untreated or ineffectively treated, cause embarrassing or distressing symptoms, affecting their quality of life. The purpose of this paper is to draw attention to this problem since it is a rare condition and therefore seldom not recognized by the general public or even by health professionals

Acute glucagon induces postprandial peripheral insulin resistance

This study was supported by Fundacao para a Ciencia e Tecnologia (FCT) grant PIC/IC/82956/2007, PTDC/BIM-MET/0486/2012, PTDC/DTP-EPI/0207/2012 and by the Portuguese Diabetes Society (SPD). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Glucagon levels are often moderately elevated in diabetes. It is known that glucagon leads to a decrease in hepatic glutathione (GSH) synthesis that in turn is associated with decreased postprandial insulin sensitivity. Given that cAMP pathway controls GSH levels we tested whether insulin sensitivity decreases after intraportal (ipv) administration of a cAMP analog (DBcAMP), and investigated whether glucagon promotes insulin resistance through decreasing hepatic GSH levels. Insulin sensitivity was determined in fed male SpragueDawley rats using a modified euglycemic hyperinsulinemic clamp in the postprandial state upon ipv administration of DBcAMP as well as glucagon infusion. Glucagon effects on insulin sensitivity was assessed in the presence or absence of postprandial insulin sensitivity inhibition by administration of L-NMMA. Hepatic GSH and NO content and plasma levels of NO were measured after acute ipv glucagon infusion. Insulin sensitivity was assessed in the fed state and after ipv glucagon infusion in the presence of GSH-E. We founf that DBcAMP and glucagon produce a decrease of insulin sensitivity, in a dose-dependent manner. Glucagon-induced decrease of postprandial insulin sensitivity correlated with decreased hepatic GSH content and was restored by administration of GSH-E. Furthermore, inhibition of postprandial decrease of insulin sensitivity L-NMMA was not overcome by glucagon, but glucagon did not affect hepatic and plasma levels of NO. These results show that glucagon decreases postprandial insulin sensitivity through reducing hepatic GSH levels, an effect that is mimicked by increasing cAMP hepatic levels and requires physiological NO levels. These observations support the hypothesis that glucagon acts via adenylate cyclase to decrease hepatic GSH levels and induce insulin resistance. We suggest that the glucagon-cAMP-GSH axis is a potential therapeutic target to address insulin resistance in pathological conditions.publishersversionpublishe