Barcelona, Spain, Thursday 19 April 2012: Exciting new data presented today at the International Liver Congress 2012 shows the gut microbiota's causal role in the development of diabetes and non-alcoholic fatty liver disease (NAFLD), independent of obesity.(1) Though an early stage animal model, the French study highlights the possibility of preventing diabetes and NAFLD with gut microbiota transplantation the engrafting of new microbiota, usually through administering faecal material from a healthy donor into the colon of a diseased recipient.(2)
In the 16 week study, two groups of germ free mice received gut microbiota transplants; one set from donor mice displaying symptoms of insulin resistance and liver steatosis (responders), the other from normal mice (non responders). The donor mice were selected due to their response to being fed a high fat diet.
The germ free group that received microbiota from symptomatic mice (responder receivers - RR) showed higher levels of fat concentration in the liver as well as being insulin resistant. The germ free group that received microbiota from healthy mice (non-responder-receivers NRR) maintained normal glucose levels and sensitivity to insulin.
EASL Scientific Committee Member Dr Frank Lammert said: "The factors leading to Non-Alcoholic Fatty Liver Disease (NAFLD) are poorly understood, but it is known that NAFLD and Type 2 diabetes are characterised, respectively, by liver inflammation and metabolic disorders like insulin resistance."
"This study shows that different microbiota cause different metabolic responses in animals. By implanting microbiota from healthy mice, the study authors prevented the development of liver inflammation and insulin resistance, both indications of liver disease and diabetes. Thus, gut microbiota transplants could have a therapeutic role in the development of these diseases."
The RR mice also showed lower levels of microorganisms than usuall
|Contact: Travis Taylor|
European Association for the Study of the Liver