21 The presents findings are consistent with those on the connection between gut microbiota, inflammation, and homeostasis, learn more and their role in the pathogenesis of obesity and related disorders,19 and 22 as well as with the findings on the relationship of diet and gut microbiota with homeostasis, as investigated in experimental models of diet-induced obesity.23 and 24 It appears that, because of the association between obesity and inflammation,25 it can be proposed that the favorable effects of probiotics in controlling inflammation may play
a role in obesity prevention and control. Among the probable mechanisms, it has been demonstrated that the modulation of the gut microbiota increases villus height and crypt depth, and leads to a thicker mucosal layer in the jejunum and in
the colon.26 These effects are due to fermentation products of bacteria, mainly short-chain fatty acids (SCFAs), such as butyrate, which acts as an energetic substrate for the colonocytes and have a trophic effect on mucosa.27 and 28 In the present study, this mechanism was highlighted, because an increase in the concentrations of protective bacteria due to the synbiotic supplementation was documented. Plasma adipocytokine levels rise with an increase in adipose tissue and adipocyte volume, except for plasma adiponectin, which is lower in obesity.29 and 30 In the present study, the increase in plasma adiponectin was
due to weight PLX3397 cost reduction and suppression of fat tissue. In conclusion, the present findings suggest the positive influence of synbiotic supplementation on inflammation factors, whose changes are dependent on weight reduction in overweight and obese children. This trial was conducted as a thesis funded by the Isfahan University of Medical Sciences, Isfahan, Iran The authors declare no conflicts of interest. This study was funded by Vice Chancellery for Research and Technology, Isfahan University of Medical Sciences, Isfahan, Iran. Guarantor: Prof. Roya Kelishadi “
“Liver transplantation is an accepted treatment GBA3 option for children with chronic liver disease, with actuarial survival rates of up to 80% in five and 75% in ten years.1 Early causes of graft failure and mortality are mostly related to vascular complications, especially hepatic artery thrombosis (HAT) and portal vein thrombosis (PVT).2 There are a number of recognized risk factors for the development of these complications in the pediatric population, such as discrepancy between donor and recipient arterial and portal diameter, surgical skills, lower recipient weight,3 and small portal vein diameter.4 There are no consistent data regarding these risk factors in the pediatric population of Brazil.