No abstract

The neurotrophin brain-derived neurotrophic factor (BDNF), which acts as a transducer, is responsible for improving cerebral stroke, neuropathic pain, and depression. Exercise can alter extracellular nucleotide levels and purinergic receptors in central nervous system (CNS) structures. This inevitably activates or inhibits the expression of BDNF via purinergic receptors, particularly the P2X receptor (P2XR), to alleviate pathological progression. In addition, the significant involvement of sensitive P2X4R in mediating increased BDNF and p38-MAPK for intracerebral hemorrhage and pain hypersensitivity has been reported. Moreover, archetypal P2X7R blockade induces mouse antidepressant-like behavior and analgesia by BDNF release. This review summarizes BDNF-mediated neural effects via purinergic receptors, speculates that P2X4R and P2X7R could be priming molecules in exercise-mediated changes in BDNF, and provides strategies for the protective mechanism of exercise in neurogenic disease.

Maternal nutrition plays a critical role in fetal growth and lifelong health outcomes. Folate is essential as a methyl donor in the epigenetic programming of offspring. Although it is critical to identify the associations between maternal folate status and child obesity, the results have been controversial. PURPOSE: This study investigates the relationship between maternal folate status and childhood obesity through meta-analysis and to examine the influence of moderating variables. METHODS: Keyword/reference search was performed in EBSCO for Academic Search Complete, Health Source-Nursing Academic Edition, Medline, SPORTDiscus database, and CINAHL. Web of Science database was also used to identify all relevant studies published in English. Meta-analysis was conducted using the CMA program to estimate the pooled effect of maternal folate status on children's obesity (BMI, BMI-Z score, or fat mass) and examine the influence of moderating variables on the overall effect. Among the 8 studies, 3 were randomized controlled trials, and 5 were cohort studies. Standardized mean difference effect size and 95% CI were computed using a random-effects model. The studies were symmetrically distributed in the funnel plot, explained the marginal possibility of publication bias. RESULTS:The better maternal folate intake, the lower the chance that the offspring will become obese: the overall ESs (Hedges' g) was .168 (95% CI = .075, .260, p = .000; small effects; cf., Cohen's criteria). Moderator analysis results revealed that the Q statistic for the age group was statistically significant (Qb = 4.730, df = 1. P = .030; explained the heterogeneity of ESs). In under 7 years, ES was .277 (95% CI =.151, .404), but, over 7 years old of age, ES was .089(95% CI =-.025,.202). However, folate concentration, ingestion volume, measure type, and method did not influence the size of the effect. CONCLUSIONS: The maternal folate status significantly affects child obesity, and the maternal folate status effect appeared to be more effective in the age of the group under 7 years. Future research should focus on the same age group, adopt systematic and field-validated maternal folate concentration or ingestion measures, and elucidate the pathways linking maternal folate status and childhood obesity outcomes.