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OBJECTIVES Yacon flour is rich in bioactive compounds (phenolic compounds and fructooligosaccharides (FOS)), and may therefore reduce the risk of diseases associated with excess body weight. However, its effect on fecal short chain fatty acids (SCFA), intestinal permeability, oxidative stress and inflammation markers has not been studied in adult humans with excess body weight. Thus, we evaluated the effect of the consumption of yacon flour on these variables. MATERIALS AND METHODS Twenty-six excess body weight (30.4 ± 2.4 kg/m2) adults (31.3 ± 8.5y) were randomized to one of two groups (yacon flour or control; n = 13) on a double blind clinical trial. Subjects received a breakfast drink containing or not yacon flour (25g) associated with an energy restricted diet, for six weeks. The flour chemical characterization, FOS and total phenolics contents were evaluated. Antioxidant capacity was evaluated in vitro and in vivo (plasma). Intestinal permeability, fecal SCFA, oxidative stress and inflammatory markers also were evaluated in vivo. RESULTS Yacon flour was well tolerated. It presented an in vitro and in vivo antioxidant capacity, increased plasma total antioxidant capacity (ΔYAC 49.16 (-4.20; 156.63)) and reduced protein carbonyl concentrations (ΔYAC -0.98 (-1.54; -0.42)). A reduction in SCFAs was observed in both groups (Δacetic -3.16 (-5.07; -0.95) vs. -1.05 (-2.65; 1.11); Δpropionic -1.05 (-2.60;-0.38) vs. -0.41 (-2.08; 0.09); Δbutyric -0.75 (-1.38; -0.04) vs. -0.28 (-0.98; 0.11), for YAC and CON, respectively). Other variables did not change. CONCLUSION The yacon flour increased the plasma antioxidant capacity, decreased oxidative stress and SCFAs in adults with obesity or overweight.OBJECTIVE Fibroblast growth factor 21 (FGF21) is among the activators that can stimulate thermogenesis in the white adipose tissue and brown adipose tissue. People with obesity have elevated blood levels of FGF21, but also develop resistance to its action, impairing its beneficial role. Inversely, clinical treatments to weight loss has been pointed out as an important therapy for increasing and recovering sensitivity to FGF21. The aim was to analyse the effect of long-term weight loss interdisciplinary intervention on FGF21 and body composition. SUBJECTS AND METHODS Eighty-six post-pubertal obese adolescents (14-19 years-old), were submitted to 20 weeks of weight loss therapy (clinical, nutritional, psychological and physical exercise support). Anthropometric measures, body composition and rest metabolic rate (RMR) by bioelectrical impedance, and serum FGF21 sample by ELISA were evaluated. The adolescents were grouped according to FGF21 individual delta variations after therapy Higher Increase (HI); lower increase (LI); lower decrease (LD); higher decrease (HD). RESULTS All groups present weight loss. Only in FGF21 ≥ 76,5 pg/mL variation the free-fat-mass and rest metabolic rate were preserved and to others group these variables were significantly reduced. CONCLUSION High increase in FGF21 can contribute to preservation of FFM and RMR after weight loss therapy, could have important implications for energy balance regulation. Future studies are necessary to continue determining the role of magnitude effects of FGF21 levels in obesity to improve clinical practice, especially in paediatrics population.OBJECTIVE This study aimed to establish the utility values of different health states associated with diabetic retinopathy in a Brazilian sample to provide input to model-based economic evaluations. SUBJECTS AND METHODS This cross-sectional study was performed in a sample of patients with type 2 diabetes mellitus (T2D) who underwent teleophthalmology screening at a primary care service from 2014 to 2016. Five diabetic retinopathy health states were defined absent, non-sight-threatening, sight-threatening, and bilateral blindness. Utility values were estimated using the Brazilian EuroQol five dimensions (EQ-5D) tariffs. Descriptive statistics were calculated. Analysis of covariance was performed to adjust the utility values for potential confounders. RESULTS The study included 206 patients. The mean (± standard deviation [SD]) utility value was 0.765 ± 0.19 (95% confidence interval [CI], 0.740-0.790). The adjusted mean utility value was 0.748 (95% CI, 0.698-0.798) in patients without diabetic retinopathy, 0.752 (95% CI, 0.679-0.825) in those with non-sight-threatening state, 0.628 (95% CI, 0.521-0.736) in those with sight-threatening state, and 0.355 (95% CI, 0.105-0.606) in those with bilateral blindness. A significant utility decrement was found between patients without diabetic retinopathy and those with a sight-threatening health state (0.748 vs. 0.628, respectively, p = 0.04). CONCLUSIONS The findings suggest that a later diabetic retinopathy health state is associated with a decrement in utility value compared with the absence of retinopathy in patients with T2D. The results may be useful as preliminary input to model-based economic evaluations. Further research is needed to investigate the impact of diabetic retinopathy on health-related quality of life in a sample more representative of the Brazilian population.Hypophosphatasia (HPP) is a rare disease with a high mortality rate in its severe forms. RI-1 nmr It is caused by mutations within the gene encoding the tissue-nonspecific alkaline phosphatase (TNSALP), an enzyme responsible for bone mineralization. In 2015, the Food and Drug Administration approved the use of asfotase alfa, the first medication showing benefit in the treatment of HPP. We describe a case with a 2-year follow-up of the first Brazilian child treated with asfotase alfa. A 5-year-old boy, born to consanguineous parents, was diagnosed with HPP at the age of 20 months. During prenatal ultrasonography, polyhydramnios and shortening of long bones were detected. After birth, he presented delayed motor development, repeated respiratory infections, and bone deformities. At the age of 2 years and 8 months, he started walking and had already lost his primary teeth. He had reduced levels of alkaline phosphatase (ALP), elevated levels of pyridoxal 5'-phosphate (PLP), and a p.Ala33Val (c.98C>T) missense mutation in homozygosis in the TNSALP gene.

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