J Physiol: damage caused by maternal microorganism mediated diet

May 29, 2019 / BIOON / - a new study published in the Journal of physiology uses a mouse model to discover that microbes in the mother's gut may cause damage to the gut barrier during pregnancy Scientists previously believed that pregnant women's metabolic changes during pregnancy were entirely caused by pregnancy hormones But now research shows that the changes of microbes living in the mother's intestines may lead to these metabolic changes If so, it offers us a therapeutic opportunity: to change this microbial community during pregnancy to improve maternal and infant health Photo source: http://cn.bing.com the gut acts as a barrier, preventing microbes and other intestinal contents from entering the blood, but in pregnant mice, more molecules can cross the barrier When pregnant mice were fed a high-fat diet, the barrier was more damaged, leading to an increase in inflammatory markers in the maternal circulation These changes in the mother may affect the development of the placenta, because the high fat diet of the mother reduces the oxygen content of the placenta The change of placenta may lead to the change of fetal development, which the author found in fetal intestine The damage of fetal intestinal development may lead to the change of intestinal function after birth, and ultimately affect the metabolism of the baby The researchers found these changes by feeding female mice high-fat food before and during pregnancy Then they studied how the gut microbiome changed They tested the mother's gut barrier by measuring how many molecules can enter the blood from the mother's gut, and then looking at how the placenta and fetus develop Deborah Sloboda, senior author of the study, said: "we are currently studying when maternal barrier functions change and how they interact with gut microbes to affect maternal metabolism and infant development "Reference materials: wajiha gohir et al, high ‐ Fat Die intake modules material internal adaptations to precedence, and results in planned hyperoxia and alternative major barrier proteins and immune markets, the Journal of Physiology (2019) Doi: 10.1113/jp277353