A obesidade é uma doença de alta prevalência no mundo e é responsável por sérias repercussões orgânicas e psicossociais, desde a infância até a vida adulta. O comportamento alimentar tem bases biológicas e sociais e, associado, à obesidade, torna-se um processo ainda mais complexo pelos aspectos psicológicos envolvidos, os quais se expressam por meio de humor depressivo, ansiedade, sentimento de culpa e, também, por mecanismos fisiológicos, como a resistência ao jejum na vigência de dietas restritivas. Há evidências de que, em indivíduos obesos, comportamentos de compulsão alimentar e ou restrição são mais freqüentes e parecem ser, em parte, responsáveis pelos fracassos observados no tratamento da obesidade. As restrições e auto-imposições das pessoas que fazem dieta, parecem ter um efeito rebote, resultando em compulsão alimentar, a qual pode associar-se a conseqüências psicológicas, como a perda da auto-estima, mudanças de humor e distração. As reflexões desta revisão sugerem que os programas para redução de peso corporal devem enfocar as bases do comportamento alimentar e desenvolver, efetivamente, ações interdisciplinares que permitam obter resultados eficazes no tratamento da obesidade.

Aim: Although previous investigators have demonstrated the presence of oxidative stress and inflammation in preeclampsia, none directly correlate both to preeclampsia. Methods: We determined in 35 preeclamptic and 35 normotensive pregnant women plasma levels of thiobarbituric acid reactive species, protein carbonyl, tumour necrosis factor-a (TNF-a), interleukin-1b (IL-1b), IL-6 and IL-10. Results: Plasma thiobarbituric acid reactive species and protein carbonyls were higher in preeclamptic patients. TNF-a and IL-6 (but not IL-1b or IL-10) were higher in preeclamptic patients. We found significant correlation between plasma IL-6 and carbonyls, and these correlated to blood pressure. Conclusions: We demonstrated that some oxidative and inflammatory mediators were altered in preeclampsia, and some correlated to blood pressure.

We suggested that in pre-eclampsia excessive arginase and low superoxide dismutase activity leads to a decrease nitric oxide levels and oxidative stress, and this may promote microvascular oxidative damage and endothelial dysfunction.

Problem. There was no direct correlation between plasma and placental oxidative damage parameters and inflammation and evidence of TLR4 pathway activation in the placenta in preeclamptic (PE) patients. Method of Study. 33 PE patients and 33 normotensive pregnant women were included. The maternal section of the placenta and blood were collected to the determination of oxidative damage markers (thiobarbituric acid reactive species and protein carbonyls), inflammatory response (interleukin-6 and myeloperoxidase activity), and activation of the TLR-4-NF-kB pathway. Results. An increase of IL-6 levels in both plasma and placenta was observed, but myeloperoxidase activity was not significantly different comparing the groups. Oxidative damage parameters were increased in plasma and placenta in PE patients. A significant increase of the protein levels of TLR-4 and NF-kB was observed in the placenta. Conclusion. The TLR4-NF-kB pathway is upregulated in PE, probably generating local and systemic inflammatory response that is followed by local and systemic oxidative damage.

The aim of this study was to determine parameters of NO metabolism in plasma and placenta of preeclamptic (PE) patients. It was conducted a case-control study at São José Hospital, Brazil. Thirty-three PE and 33 normotensive pregnant were included in the study. The diagnosis of PE was established in accordance with the definitions of American College of Obstetricians and Gynecologists. Peripheral venous blood and placenta samples were obtained at postpartum period. Plasma NO levels and SOD activity were significantly lower and endothelin-1 levels and arginase activity were significantly higher in PE women when compared to controls. None of the analyzed parameters were different in the placenta between groups. Our findings suggest that parameters associated with NO metabolism are altered only at the systemic level, but not in placenta of PE patients.