Scope: Coconut oil (CO) diets remain controversial due to the possible association with metabolic disorder and obesity. This study investigates the metabolic effects of a low amount of CO supplementation. Methods and Results: Swiss male mice are assigned to be supplemented orally during 8 weeks with 300 µL of water for the control group (CV), 100 or 300 µL of CO (CO100 and CO300) and 100 or 300 µL of soybean oil (SO; SO100 and SO300). CO led to anxious behavior, increase in body weight gain, and adiposity. In the hypothalamus, CO and SO increase cytokines expression and pJNK, pNFKB, and TLR4 levels. Nevertheless, the adipose tissue presented increases macrophage infiltration, TNF-and IL-6 after CO and SO consumption. IL-1B and CCL2 expression, pJNK and pNFKB levels increase only in CO300. In the hepatic tissue, CO increases TNF-and chemokines expression. Neuronal cell line (mHypoA-2/29) exposed to serum from CO and SO mice shows increased NFKB migration to the nucleus, TNF-, and NFKBia expression, but are prevented by inhibitor of TLR4 (TAK-242). Conclusions: These results show that a low-dose CO changes the behavioral pattern, induces inflammatory pathway activation, TLR4 expression in healthy mice, and stimulates the pro-inflammatory response through a TLR4-mediated mechanism.

Background and objectives Strontium ranelate is a medication indicated for the treatment of osteoporosis that presents concomitant anti‐resorptive and osteoanabolic dual biological activity. However, the effects of strontium ranelate on alveolar bone have been poorly explored. Furthermore, to date, there are no data on the effects of this medication on alveolar bone loss (BL) during conditions of estrogen deficiency. Therefore, the aim of this study was to evaluate the effects of strontium ranelate on ligature‐induced periodontitis in estrogen‐deficient and estrogen‐sufficient rats. Methods Ninety‐six rats were assigned to one of the following groups: sham‐surgery + water (estrogen‐sufficient; n = 24); ovariectomy + water (estrogen‐deficient; n = 24), sham‐surgery + strontium ranelate (ranelate/estrogen‐sufficient; n = 24) and; ovariectomy + strontium ranelate (ranelate/estrogen‐deficient; n = 24). The rats received strontium ranelate or water from the 14th day after ovariectomy until the end of the experiment. On the 21st day after ovariectomy, one first mandibular molar received a ligature, while the contralateral tooth was left unligated. Eight rats per group were killed at 10, 20, and 30 days after ligature placement. Bone loss (BL) and trabecular bone area (TBA) were analyzed in the furcation area of ligated and unligated teeth at all experimental times by histometry. Tartrate‐resistant acid phosphatase (TRAP) positive cells and immunohistochemical staining for osteocalcin (OCN), osteopontin (OPN), osteoprotegerin (OPG), and receptor activator of NF‐КB ligand (RANKL) were assessed in the ligated teeth at 30 days after ligature placement. Results At 10 and 30 days, ligated teeth of the estrogen‐deficient group exhibited higher BL, when compared to all other groups (P < .05). At 10 days, TBAs were higher in the unligated teeth of strontium ranelate‐treated groups, when compared to those of untreated groups (P < .05). At 30 days, the ligated teeth of the estrogen‐deficient group exhibited lower TBA than the other groups (P < .05). There were no differences among groups regarding the number of TRAP‐stained cells (P < .05). The strontium ranelate‐treated groups exhibited lower expressions of OCN and RANKL than the untreated groups (P < .05). The estrogen‐sufficient group presented higher staining for OPG than both treated and untreated estrogen‐deficient groups (P < .05). Conclusions Strontium ranelate prevented ligature‐induced BL in an estrogen‐deficiency condition and, to a certain extent, increased TBA in the presence and absence of periodontal collapse in states of estrogen deficiency and estrogen sufficiency. Furthermore, strontium ranelate also affected the expression of bone markers, appearing to have acted predominantly as an anti‐resorptive agent.

Non-pharmacologic treatments of Sleep-Related Movement Disorders (SRMD) are already well described in the literature. The physical activity has been presented as a factor to improve quality of life and in several aspects related to sleep disorders. Thus, the purpose of this review was to analyze the benefits of physical exercise and your indication to improve to SRMD. In the research, 19 studies were found that evaluate the efficacy of physical exercise on SRMD in both human and animal models. The results demonstrate that both acute and chronic physical exercises are effective in reducing symptoms of SRMD. However, most studies were performed with aerobic exercise. Three studies evaluated the efficacy of combined exercise, and no studies have investigated the relationship of resistance exercise. Regarding the mechanisms involved, a study discusses the relationship between the release of beta-endorphin and the exercise practice, and two studies with animal models show the changes of the dopaminergic system after physical exercise. From this evidences, we suggested that physical exercise is a favorable non-pharmacological treatment for SRMD. However, more studies should be available for a better understanding of the molecular mechanisms involved, as well of the type, duration and better time of the day to practice.

RESUMO Introdução: O exercício físico gera resultados positivos para a qualidade do sono e atua no ciclo sono-vigília por meio de seu efeito sincronizador indireto do relógio biológico. Objetivo: Avaliar a qualidade de sono, o cronotipo e o desempenho de corredores amadores de rua da cidade de Limeira. Métodos: Foram avaliados 42 indivíduos de ambos os sexos (28 ± 1,47 anos), que praticavam corrida de rua. O instrumento utilizado para aplicação dos questionários foi a plataforma Google Drive - Google Forms. Foram formuladas questões que englobam o cotidiano de um corredor de rua e também questionários para avaliação do cronotipo, sonolência e qualidade do sono. Resultados: Os resultados demonstraram que o cronotipo mais frequente foi o matutino (47,61%), seguido por intermediário (30,95%) e vespertino (21,42%). A frequência de corridas foi 88% no período da manhã, 9% no período da noite e 4% período da tarde. Com relação à qualidade de sono geral foi verificado que 59% dos corredores tinham má qualidade de sono. Ao analisar as variáveis de sono e sonolência em decorrência do horário da última corrida realizada, verificou-se que as pessoas que correram no período da tarde tiveram pior qualidade do sono e os que correram à noite tiveram índices de sonolência. Não se encontrou diferença no desempenho das corridas de 5 km entre matutinos e vespertinos; no entanto, constatou-se fraca associação entre o tempo da última corrida e a pontuação do cronotipo, demonstrando que os matutinos realizavam as provas em menor tempo. Conclusão: Assim, podemos sugerir que o cronotipo e o padrão de sono podem interferir no desempenho e, dessa forma, devem ser levados em conta durante os treinamentos.

The gene that encodes the protein tyrosine phosphatase D (PTPRD) may be related to brain circuits associated with sleep, and has been seen as an interesting molecule, a “druggable” drug target. This gene is a potential candidate for increasing therapeutic advances in restless legs syndrome, a sleep‐related movement disorder, that manifests as an uncontrollable desire to move limbs (legs) to relieve uncomfortable sensations. Changes in the PTPRD gene expression may increase the chance of developing this syndrome. Treatment with pramipexole is used in restless legs syndrome. This study aims to verify the effect of treatment with pramipexole on the PTPRD expression, as well as on the sleep pattern in an animal model for restless legs syndrome. For this, an animal model of sleep‐related movement disorders (spontaneously hypertensive rats) was distributed in groups: (a) spontaneously hypertensive rats−control; (b) spontaneously hypertensive rats−pramipexole (0.125 mg kg−1 for 4 weeks). The analyses of PTPRD gene and protein expression were performed in the striatum and spinal cord by quantitative real‐time polymerase chain reaction and indirect enzyme‐linked immunosorbent assay, respectively. Electrocorticographic and electromyographic analyses were performed. There was no difference in the PTPRD mRNA levels, as well as in the protein levels, although a tendency has been observed for decreased gene expression in the striatum and increased protein expression in the spinal cord in the spontaneously hypertensive rats−pramipexole group. Pramipexole improved the animals' sleep pattern. Thus, the treatment with pramipexole in the evaluated dose and time tended to alter the expression of the PTPRD protein in the spinal cord, in addition to significantly improving the sleep pattern.