Proinflammatory and oxidative stress markers in patients submitted to Roux-en-Y gastric bypass after 1 year of follow-up.

BACKGROUND/OBJECTIVES: This study examined the effect of weight loss after 3, 6 and 12 months of Roux-en-Y Gastric Bypass (RYGB) on energy intake and on several biomarkers of oxidative stress such as levels of vitamin C, beta-carotene, vitamin E (diet/blood), nitric oxide metabolites (NOx), myeloperoxidase (MPO), thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) and activity of catalase (CAT). SUBJECTS/METHODS: Study with a control group (CG), assessed once, and a bariatric group (BG) assessed at the basal period as well as at 3, 6 and 12 months post-surgery; both groups were composed of 5 men and 31 women (n=36). Age was 38.7 ± 9.4 and 39.6 ± 9.2 years old and body mass index (BMI) was 22.2 0 ± 2.1 and 47.6 ± 9.1 kg/m(2), respectively. The variance measure quoted was SEM. RESULTS: The body weight at 12 months was 35.8 ± 1.0% (P<0.001) lower than that of the basal period. At the basal period BG showed higher levels of NOx (P=0.007) and TBARS (P<0.001) and lower levels of vitamins C and E (P<0.001) compared with CG. After 3 months the activity of MPO was decreased (P<0.001). Six months after surgery GSH levels were decreased (P=0.037), whereas CAT activity was increased (P=0.029). After 12 months levels of NOx (P=0.004), TBARS (P<0.001), beta-carotene (P<0.001) and vitamin E (P<0.001) were decreased, whereas those of vitamin C (P<0.001) were increased compared with controls. CONCLUSION: RYGB followed by a daily vitamin supplement apparently attenuated pro-inflammatory and oxidative stress markers 1 year after surgery, but additional antioxidant supplementation appears necessary.

The interface between obesity and periodontitis with emphasis on oxidative stress and inflammatory response.

Obesity is characterized by the abnormal or excessive deposition of fat in the adipose tissue. Its consequences go far beyond adverse metabolic effects on health, causing an increase in oxidative stress that leads not only to endothelial dysfunction but also to negative effects in relation to periodontitis, because of the increase in proinflammatory cytokines. Thus, obesity appears to participate in the multifactorial phenomenon of causality of periodontitis through the increased production of reactive oxygen species. Within this context, this paper aims to highlight, by analysis and description of previous studies, the interface between obesity and periodontitis, with emphasis on oxidative stress and the inflammatory response.