ABSTRACT
OBJECTIVE: The aim of this study was to evaluate overall genetic damage induced by total sleep deprivation in obese, female Zucker rats of differing ages. METHOD: Lean and obese Zucker rats at 3, 6, and 15 months old were randomly distributed into two groups for each age group: home-cage control and sleep-deprived (N = 5/group). The sleep-deprived groups were deprived sleep by gentle handling for 6 hours, whereas the home-cage control group was allowed to remain undisturbed in their home-cage. At the end of the sleep deprivation period, or after an equivalent amount of time for the home-cage control groups, the rats were brought to an adjacent room and decapitated. The blood, brain, and liver tissue were collected and stored individually to evaluate DNA damage. RESULTS: Significant genetic damage was observed only in 15-month-old rats. Genetic damage was present in the liver cells from sleep-deprived obese rats compared with lean rats in the same condition. Sleep deprivation was associated with genetic damage in brain cells regardless of obesity status. DNA damage was observed in the peripheral blood cells regardless of sleep condition or obesity status. CONCLUSION: Taken together, these results suggest that obesity was associated with genetic damage in liver cells, whereas sleep deprivation was associated with DNA damage in brain cells. These results also indicate that there is no synergistic effect of these noxious conditions on the overall level of genetic damage. In addition, the level of DNA damage was significantly higher in 15-month-old rats compared to younger rats.
Subject(s)
Animals , Female , Rats , DNA Damage , Obesity/genetics , Sleep Deprivation/genetics , Age Factors , Brain/physiopathology , Comet Assay , Liver/physiopathology , Obesity/physiopathology , Random Allocation , Rats, Zucker , Sleep Deprivation/complications , Sleep Deprivation/physiopathology , Time FactorsABSTRACT
O objetivo do presente estudo foi avaliar os efeitos interativo e respectivo do treinamento fÍsico moderadode natação e da dieta hiperlipídica sobre o metabolismo de carboidratos e lipídeos no período de recuperação ao exercício em ratos machos adultos. Os animais foram divididos em sedentários (S) e treinados (T). O treinamento consistiu de natação a 90 min/dia, cinco dias/semana. Cada grupo foi subdividido em dieta padrão normocalórica (N) e dieta hipercalórica/hiperlipídica (H). Depois de oito semanas, os animais dos quatro grupos (SN, TN, SH e TH) foram sacrificados em repouso ou uma e duas horas após o exercício. A dieta hipercalórica (grupo SH vs. SN) aumentou o peso dos tecidos adiposos brancos, a glicemia, a concentração plasmática de triglicerídeos e de colesterol total e diminuiu o conteúdo de glicogínio. Por outro lado, o treinamento moderado de natação (grupo TN vs. SN) diminuiu o peso dos tecidos adiposos brancos e melhorou o metabolismo de carboidratos, aumentando o conteúdo de glicogínio. Quando associados (grupo TH vs. SH e TN), o treinamento não foi capaz de reverter os efeitos da dieta para o peso dos tecidos adiposos brancos, conteúdo de glicogínio e glicemia. Com relação ao período de recuperação, concluímos que os efeitos benéficos do treinamento em promover uma rápida recuperação dos substratos endógenos, principalmente reposição de glicogínio, são prejudicados pela dieta hiperlipídica associada ao treinamento.