BackgroundPhysical exercise induces positive alterations in gene expression involved in the metabolism of obesity. Maternal exercise provokes adaptations soon after birth in the offspring. Here, we investigated whether adult mouse offspring of swim-trained mothers is protected against the development of the deleterious effects of high fat diet (HFD).MethodsOur study comprises two parts. First, female C57BL/6 mice were divided into one sedentary and one swim-trained group (before and during pregnancy, n = 18). In the second part, adult offspring (n = 12) of trained and sedentary mothers was challenged to HFD for 16 weeks. Notably, most of the analysis was done in male offspring.ResultsOur results demonstrate that maternal exercise has several beneficial effects on the mouse offspring and protects them from the deleterious effects of HFD in the adult. Specifically, swimming during pregnancy leads to lower birth weight in offspring through 2 months of age. When subjected to HFD for 4 month in the adulthood, our study presents novel data on the male offspring’s metabolism of trained mothers. The offspring gained less weight, which was accompanied by less body fat, and they used more calories during daytime compared with offspring of sedentary mothers. Furthermore, we observed increased adiponectin expression in skeletal muscle, which was accompanied by decreased leptin levels and increased insulin sensitivity. Decreased interleukin-6 expression and increased peptide PYY levels were observed in sera of adult offspring of mothers that swam during pregnancy.ConclusionsOur results point to the conclusion that maternal exercise is beneficial to protect the offspring from developing obesity, which could be important for succeeding generations as well.Electronic supplementary materialThe online version of this article (doi:10.1186/s12986-015-0052-z) contains supplementary material, which is available to authorized users.
Laser photobiomodulation reduced skeletal muscle edema as well as cytokines and CRP, leading to a significant reduction in inflammatory markers.
Purpose Verify the influences of physical activity level, nutritional status and screen habits on the prevalence of back pain in Brazilian students. Methods The sample consisted of 577 schoolchildren (female = 274; male = 303) aged between 10 and 16 years old, regularly enrolled in the 6 th grade of elementary school living in the metropolitan area of the Alto Tietê of the state of São Paulo, Brazil. The prevalence, intensity and frequency of pain was verified with the Back Pain Assessment Instrument. The usual practice of physical activity was verified with the Physical Activity Questionnaire for Older Children/Adolescent. Nutritional status was analyzed using Body Mass Index. Screen habits were obtained through a previously structured questionnaire. Results The Chi-square test indicated that pain complaint and its prevalence in the cervical region are significantly higher in females (p < 0.05). The multiple logistic regression test revealed that watching television influences the prevalence of cervical pain and that the use of more than one screen increases the occurrence of low back pain in male students (p < 0.05). Conclusion Female students were the most affected by back pain complain, especially in the cervical region. However, factors associated with the prevalence of back pain were found only in males.
Angiotensin-I-converting enzyme (ACE) is involved in the synthesis and degradation of important bioactive peptides. The ACE gene has a 287-bp insertion/deletion polymorphism that controls ACE expression through a mechanism that remains elusive. In this study, we found that the 287-bp polymorphic element of the ACE gene, a member of the AluYa5 sub-family of Alu elements, codes for an RNA molecule that controls the levels of ACE mRNA. Transient transfection of a plasmid containing a CMV promoter upstream of the ACE polymorphic element resulted in significant expression of an AluYa5 RNA and reduced ACE mRNA expression as well as ACE enzymatic activity in AD 293 cells. The AluYa5 element also independently reduced the expression of other genes, regardless of whether these genes harbored Alu elements within their genomic context. Interestingly, the CMV promoter was not required for the expression of the AluYa5 element in AD 293 cells. The 287-bp sequence was sufficient to produce AluYa5 RNA and led to a significant reduction in ACE gene expression. Moreover, the removal of an 11-bp fragment of the 3' end of the ACE polymorphic sequence, which is specific to this particular AluYa5 element, did not prevent this element from being expressed but did affect its ability to target ACE expression. Thus, the expression of the AluYa5 polymorphic element within the ACE gene could explain why patients carrying the ACE insertion polymorphism have reduced risk of developing several chronic diseases.
We conclude that the kinin B2 receptor does not have a protective role in renal injury.
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