Fredrik Bäckhed

The microbes in our intestines out number our human cells in the body with an order of magnitude. The microbial genes (microbiome) complement our own genome and affect our physiology and metabolism. I have shown that germ-free mice are resistant to developing diet-induced obesity. In order to study whether the microbial community or its functional capacity (metagenome) is altered in these metabolic diseases we assess the metagenomes of well-pheontyped patients using next-generation sequencing. By rederiving genetically engineered mice as germ-free we are delineating the molecular mechanisms by which the gut microbiota causes disease.

My main focus now is to delineate the mechanisms by which the gut microbiota modualtes host physiology and metabolism and whether the gut microbiota may be a target for preventing or treating metabolic disease.