Influência da restrição aguda de sono no controle neuroendócrino da ingestão alimentar e metabolismo de indivíduos obesos.
Arquivos
Data
2012
Autores
Zimberg, Ioná Zalcman 
Orientadores
Mello, Marco Tulio de
Tipo
Tese de doutorado
Título da Revista
ISSN da Revista
Título de Volume
Resumo
Objetivo: O presente estudo teve como objetivo analisar as respostas neuroendocrinas, metabolicas e polissonograficas de individuos obesos e eutroficos submetidos a restricao do inicio e final do sono. Metodos: Quinze adultos jovens saudaveis (26,63±2,68 anos) do sexo masculino, sendo 7 obesos (IMC: 33,43±2,84) e 8 com peso normal (IMC: 22,22±2,54), participaram de 3 condicoes de sono crossover randomizadas com 3 noites de duracao, sendo: sono normal (sono: 23-07h), restricao do inicio do sono (RIS) (sono: 03-07h) e restricao do final do sono (RFS) (sono: 23-03h). Em cada condicao, os voluntarios permaneceram 4 dias no laboratorio. Durante a permanencia no laboratorio, foram oferecidas 3 refeicoes normocaloricas ao longo do dia. No terceiro dia de cada condicao, a partir das 07:00 horas, foram iniciadas as coletas de sangue, que se repetiram a cada 1 hora durante 24 horas. Foram analisadas as concentracoes de glicose, insulina, peptideo C, colesterol total e fracoes, triacilglicerol, acidos graxos livres nao-esterificados (NEFA), cortisol, adiponectina, TNF-α, IL-6, proteina C reativa, leptina, grelina total e grelina acilada. No quarto dia, as 07:00 horas foi realizada a medida da taxa metabolica basal. Resultados: No grupo obesidade foram verificadas as seguintes modificacoes estatisticamente significantes: aumento da concentracao de cortisol no periodo da noite e reducao de manha apenas na RFS, aumento da concentracao de leptina ao longo das 24 horas da RIS e no periodo da manha da RFS. No grupo peso normal foram observadas as seguintes modificacoes estatisticamente significantes: reducao da tolerancia a glicose noturna em conjunto com a elevacao da concentracao de insulina e peptideo C em resposta ao cafe da manha na RFS, aumento das concentracoes de IL-6 no periodo da noite na RIS e ao longo das 24 horas na RFS, reducao das concentracoes de grelina total na RIS e RFS e da grelina acilada na RFS. Em ambos os grupos foram verificadas as seguintes modificacoes estatisticamente significantes: reducao das concentracoes de colesterol total e fracoes, triacilglicerol e NEFA na RIS e RFS, reducao das concentracoes de TNF-α no periodo da noite na RIS e RFS e aumento da concentracao de adiponectina na RIS. Verificou-se que a taxa metabolica basal aumentou significantemente na condicao de RFS do grupo obesidade. Conclusao: A restricao de sono por tres noites levou a modificacoes neuroendocrinas e metabolicas distintas entre os grupos avaliados mas que sugerem prejuizo no metabolismo glicidico e lipidico, inflamacao e alteracao dos neuropeptideos associados ao controle do comportamento alimentar, que poderia predispor a resistencia a insulina e doencas cardiometabolicas. Esses dados contribuem para o aprofundamento das multiplas vias metabolicas que ligam a restricao de sono a obesidade
Aim: This study aimed to analyze the neuroendocrine, metabolic and polysomnographic of obese and normal-restricted the beginning and end of sleep. Methods: Fifteen healthy young male adults (26.63±2.68 years), 7 obese (BMI: 33.43±2.84) and 8 normal weight (BMI: 22.22±2.54), were subjected to three crossover randomized conditions of sleep for three consecutive nights: normal sleep (bedtime: 23:00h – 7:00h); restriction at the beginning of the night (RBN) (bedtime: 3:00h – 7:00h); and restriction at the end of the night (REN) (bedtime: 23:00h – 3:00h). In each condition volunteers remained in the laboratory for four days. Three normocaloric meals were offered during the day while in the laboratory. On the third day of each condition, at 07:00 hours blood samples were collected at 1-h intervals over the course of 24 h. Concentrations of glucose, insulin, C-peptide, total cholesterol and fractions, triacilglicerol, non-esterified free fatty acids (NEFA), cortisol, adiponectin, TNF-α, IL-6, C-reactive protein, leptin, total and acylated ghrelin were analyzed. On the fourth day of each condition, basal metabolic rate was measured at 07:00 hours. Results: In obese group it was verified the following statistically significant modifications: cortisol concentration increased in the evening and decreased in the morning only in REN, leptin concentration increased throughout the 24 hours in RBN and in the morning of the REN. In the normal weight group the following statistically significant changes were seen: glucose tolerance reduced in the evening and insulin and C-peptide concentrations increased in response to breakfast in REN, IL-6 concentration increased in the evening in RBN and over 24 hours in the REN, total ghrelin concentration reduced in RBN and REN and acylated ghrelin concentration reduced in RFS. In both groups, the following statistically significant changes were observed: total cholesterol and fractions, triacylglycerol and NEFA reduced in RBN and REN, TNFα concentration reduced during the night in RBN and REN, and adiponectin concentration increased in RBN. Basal metabolic rate was significantly increased in REN in obese group. Conclusions: 3 nights of sleep restriction led to different metabolic and neuroendocrine changes in groups evaluated. Taken together, these data suggest that sleep restriction can impair glucose and lipid metabolism, increase inflammation and alter the neuropeptides associated with control of hunger, which could predispose to insulin resistance and cardiometabolic diseases. These physiological changes are important for the further development of multiple metabolic pathways linking sleep restriction and obesity
Aim: This study aimed to analyze the neuroendocrine, metabolic and polysomnographic of obese and normal-restricted the beginning and end of sleep. Methods: Fifteen healthy young male adults (26.63±2.68 years), 7 obese (BMI: 33.43±2.84) and 8 normal weight (BMI: 22.22±2.54), were subjected to three crossover randomized conditions of sleep for three consecutive nights: normal sleep (bedtime: 23:00h – 7:00h); restriction at the beginning of the night (RBN) (bedtime: 3:00h – 7:00h); and restriction at the end of the night (REN) (bedtime: 23:00h – 3:00h). In each condition volunteers remained in the laboratory for four days. Three normocaloric meals were offered during the day while in the laboratory. On the third day of each condition, at 07:00 hours blood samples were collected at 1-h intervals over the course of 24 h. Concentrations of glucose, insulin, C-peptide, total cholesterol and fractions, triacilglicerol, non-esterified free fatty acids (NEFA), cortisol, adiponectin, TNF-α, IL-6, C-reactive protein, leptin, total and acylated ghrelin were analyzed. On the fourth day of each condition, basal metabolic rate was measured at 07:00 hours. Results: In obese group it was verified the following statistically significant modifications: cortisol concentration increased in the evening and decreased in the morning only in REN, leptin concentration increased throughout the 24 hours in RBN and in the morning of the REN. In the normal weight group the following statistically significant changes were seen: glucose tolerance reduced in the evening and insulin and C-peptide concentrations increased in response to breakfast in REN, IL-6 concentration increased in the evening in RBN and over 24 hours in the REN, total ghrelin concentration reduced in RBN and REN and acylated ghrelin concentration reduced in RFS. In both groups, the following statistically significant changes were observed: total cholesterol and fractions, triacylglycerol and NEFA reduced in RBN and REN, TNFα concentration reduced during the night in RBN and REN, and adiponectin concentration increased in RBN. Basal metabolic rate was significantly increased in REN in obese group. Conclusions: 3 nights of sleep restriction led to different metabolic and neuroendocrine changes in groups evaluated. Taken together, these data suggest that sleep restriction can impair glucose and lipid metabolism, increase inflammation and alter the neuropeptides associated with control of hunger, which could predispose to insulin resistance and cardiometabolic diseases. These physiological changes are important for the further development of multiple metabolic pathways linking sleep restriction and obesity
Descrição
Citação
ZIMBERG, Ioná Zalcman. Influência da restrição aguda de sono no controle neuroendócrino da ingestão alimentar e metabolismo de indivíduos obesos. 2012. 143 f. Tese (Doutorado) - Escola Paulista de Medicina, Universidade Federal de São Paulo. São Paulo, 2012.