Data from: Intestinal Ralstonia pickettii augments glucose intolerance in obesity

An altered intestinal microbiota composition has been implicated in the
pathogenesis of metabolic disease including obesity and type 2 diabetes
mellitus (T2DM). Low grade inflammation, potentially initiated by the
intestinal microbiota, has been suggested to be a driving force in the
development of insulin resistance in obesity. Here, we report that
bacterial DNA is present in mesenteric adipose tissue of obese but
otherwise healthy human subjects. Pyrosequencing of bacterial 16S rRNA
genes revealed that DNA from the Gram-negative species Ralstonia was most
prevalent. Interestingly, fecal abundance of Ralstonia pickettii was
increased in obese subjects with pre-diabetes and T2DM. To assess if R.
pickettii was causally involved in development of obesity and T2DM, we
performed a proof-of-concept study in diet-induced obese (DIO) mice.
Compared to vehicle-treated control mice, R. pickettii-treated DIO mice
had reduced glucose tolerance. In addition, circulating levels of
endotoxin were increased in R. pickettii-treated mice. In conclusion, this
study suggests that intestinal Ralstonia is increased in obese human
subjects with T2DM and reciprocally worsens glucose tolerance in DIO mice.