Fructooligosaccharides and galactooligosaccharides improve hepatic steatosis via gut microbiota-brain axis modulation.

Studies have shown that gut dysbiosis is associated with the steatotic liver disease associated with metabolic dysfunction (MALSD) and its severity. This study evaluated the effects of two commercially available prebiotics fructooligosaccharides (FOS) and galactooligosaccharides(GOS) on hepatic adipogenesis, inflammation, and gut microbiota in high-fat diet-induced MALSD. The results indicated that FOS and GOS effectively reduced insulin resistance, hyperglycaemia, triglyceridemia, cholesterolaemia, and IL-1ß serum levels. Moreover, FOS and GOS modulated the lipogenic (SREBP-1c, ACC, and FAS) and lipolytic (ATGL) signalling pathways, and reduced inflammatory markers such as p-NFκB-65, IL-6, iNOS, COX-2, TNF-α, IL-1ß, and nitrotyrosine. FOS and GOS also enhanced the abundance of acetate producers' bacteria Bacteroides acidifaciens and Bacteroides dorei. FOS and GOS also induced positive POMC/GPR43 neurons at the arcuate nucleus, indicating hypothalamic signalling modulation. Our results suggest that FOS and GOS attenuated MALSD by reducing the hepatic lipogenic pathways and intestinal permeability through the gut microbiota-brain axis.

Mesenteric ischemia as a cause of early death among mice infected by Schistosoma mansoni

Laboratory maintenance of the Schistosoma mansoni cycle is necessary for developing studies regarding the diagnosis, treatment and control of schistosomiasis. Within this perspective, it is paramount that mice infected by the parasite should present a minimum survival of six months. However, between October 2016 and May 2017, early deaths were observed among infected animals kept in the vivarium of the Schistosomiasis Reference Service of IAMFIOCRUZ. Therefore, the purpose of the present study was to present the results obtained after investigating the main cause of death among these animals. To achieve this, animals that died or that needed to be euthanized due to clinical distress caused by parasite infection were necropsied to investigate the cause of death and clinical condition. Fragments from the intestines, mesenteric vessels and livers were removed and were subjected to histopathological studies. In addition, mouse feces were collected and analyzed using the hydrogen peroxide reaction to detect occult blood. Over an eight-month period, 70 deaths were noted. Forty two animals presented mesenteric ischemia, a vascular insufficiency syndrome that causes a reduction in the nutrient supply to the intestinal viscera. There is, therefore, a need to reduce the infective parasite load in mice to increase their survival, reduce distress caused by the infection and ensure maintenance of the S. mansoni cycle, thus enabling continuity of scientific studies on this parasitosis.