Wu got his PhD degree from James D. Watson Institute of Genome Sciences,
Zhejiang University in 2012. He is currently working as a bioinformatician in
Fredrik Backhed’s Lab where he focuses more on how to understand host-microbes
interactions within the context of metabolic disorders by integrating multi-omics
datasets. His work on low carbs diet- and metformin-microbiota interactions
have been published in Cell Metabolism and Nature Medicine recently.
From multi-omics to causality: time to go for human
The Wallenberg Laboratory, Sahlgrenska University
Hospital, University of Gothenburg, Sweden
links between human health and gut microbes have been well established but the
causality and molecular mechanisms behind those links remain elusive. By multi-omics
profiling in two recent human intervention studies, we found: 1) the
glucose-lowering effect of orally administrated metformin is partially due to
metformin-adapted microbial changes and this drug may interact with bacteria by
regulating metal-chelating proteins; 2) carbohydrate-restricted diet can drive
microbial shifts toward folate production which in turn explains 20-30% of
liver fat reduction potentially through folate-mediated one-carbon metabolism.
In a third omics study, we found that a new bacterial metabolite imidazole
propionate (ImP, derived from histidine metabolism) which has higher
circulating levels in individuals with T2D can directly lead to insulin
resistance when injected to mice. We are now designing short-term human
intervention studies trying to address whether histidine-rich protein diet can result
in increased circulating ImP and whether levels of this metabolite depend on
the individual settings of the gut microbiome.