Daily light exposure, sleep-wake cycle and attention in adolescents from different urban contexts.

OBJECTIVE: to compare daily light exposure, activity-rest rhythm, sleep-wake cycle (SWC) and attention in Brazilian students living in different levels of urbanization. METHODS: 115 adolescents (74 girls), aged 14-18 years (mean 15.5 ± 0.7 years), from the first years of high school have participated. The SWC was evaluated by actimetry and a Sleep Diary for 10 days. Besides, the "Health and Sleep" Questionnaire, the Morningness and Eveningness Scale for adolescents, the Pittsburgh Sleep Quality Index, and the Pediatric Daytime Sleepiness Scale were answered. Attention was assessed by a Continuous Performance Task. RESULTS: In the less urbanized region, there were a greater exposure to light during the day accompanied by a higher proportion of morning-types and less occurrence of excessive daytime sleepiness. Otherwise, in the more urbanized region, adolescents showed a trend to sleep less in weekdays and presented more irregularity in sleep duration between weekdays and weekend, with 83 ± 15% of sleep efficiency, 01:04 ± 1:30 h of WASO and 7 ± 6.7 awakenings per night on the weekdays, suggestive of poor sleep quality. Despite of this, they showed better attentional performance: more correct responses (tonic and phasic alertness, and sustained attention) and less omissions (for all components). Regardless of the degree of urbanization, there was partial sleep deprivation, irregular sleep schedules and poor sleep quality in adolescents. CONCLUSIONS: The daily light exposure and activity-rest profiles, SWC and attention in adolescents varied according to the degree of urbanization. Besides, the negative impacts of early school starting times leading to sleep deprivation, irregular sleep times and poor sleep quality were observed irrespective of the degree of urbanization, reinforcing that the early school starting time at morning is a strong temporal challenge for teenagers, having negative impacts on cognition and academic performance.

The Anti-atherogenic Role of Exercise Is Associated With the Attenuation of Bone Marrow-Derived Macrophage Activation and Migration in Hypercholesterolemic Mice.

An early event in atherogenesis is the recruitment and infiltration of circulating monocytes and macrophage activation in the subendothelial space. Atherosclerosis subsequently progresses as a unresolved inflammatory disease, particularly in hypercholesterolemic conditions. Although physical exercise training has been a widely accepted strategy to inhibit atherosclerosis, its impact on arterial wall inflammation and macrophage phenotype and function has not yet been directly evaluated. Thus, the aim of this study was to investigate the effects of aerobic exercise training on the inflammatory state of atherosclerotic lesions with a focus on macrophages. Hypercholesterolemic LDL-receptor-deficient male mice were subjected to treadmill training for 8 weeks and fed a high-fat diet. Analyses included plasma lipoprotein and cytokine levels; aortic root staining for lipids (oil red O); macrophages (CD68, MCP1 and IL1ß); oxidative (nitrotyrosine and, DHE) and endoplasmic reticulum (GADD) stress markers. Primary bone marrow-derived macrophages (BMDM) were assayed for migration activity, motility phenotype (Rac1 and F-actin) and inflammation-related gene expression. Plasma levels of HDL cholesterol were increased, while levels of proinflammatory cytokines (TNFa, IL1b, and IL6) were markedly reduced in the exercised mice. The exercised mice developed lower levels of lipid content and inflammation in atherosclerotic plaques. Additionally, lesions in the exercised mice had lower levels of oxidative and ER stress markers. BMDM isolated from the exercised mice showed a marked reduction in proinflammatory cytokine gene expression and migratory activity and a disrupted motility phenotype. More importantly, bone marrow from exercised mice transplanted into sedentary mice led to reduced atherosclerosis in the recipient sedentary mice, thus suggesting that epigenetic mechanisms are associated with exercise. Collectively, the presented data indicate that exercise training prevents atherosclerosis by inhibiting bone marrow-derived macrophage recruitment and activation.

Coenzyme Q10 protects against ß-cell toxicity induced by pravastatin treatment of hypercholesterolemia.

New onset of diabetes is associated with the use of statins. We have recently demonstrated that pravastatin-treated hypercholesterolemic LDL receptor knockout (LDLr-/- ) mice exhibit reductions in insulin secretion and increased islet cell death and oxidative stress. Here, we hypothesized that these diabetogenic effects of pravastatin could be counteracted by treatment with the antioxidant coenzyme Q 10 (CoQ 10 ), an intermediate generated in the cholesterol synthesis pathway. LDLr -/- mice were treated with pravastatin and/or CoQ 10 for 2 months. Pravastatin treatment resulted in a 75% decrease of liver CoQ 10 content. Dietary CoQ 10 supplementation of pravastatin-treated mice reversed fasting hyperglycemia, improved glucose tolerance (20%) and insulin sensitivity (>2-fold), and fully restored islet glucose-stimulated insulin secretion impaired by pravastatin (40%). Pravastatin had no effect on insulin secretion of wild-type mice. In vitro, insulin-secreting INS1E cells cotreated with CoQ 10 were protected from cell death and oxidative stress induced by pravastatin. Simvastatin and atorvastatin were more potent in inducing dose-dependent INS1E cell death (10-15-fold), which were also attenuated by CoQ 10 cotreatment. Together, these results demonstrate that statins impair ß-cell redox balance, function and viability. However, CoQ 10 supplementation can protect the statins detrimental effects on the endocrine pancreas.