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Intestinal Ralstonia pickettii augments glucose intolerance in obesity.

Shanthadevi D Udayappan1, Petia Kovatcheva-Datchary2, Guido J Bakker1

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Summary

Bacterial DNA, particularly Ralstonia, was found in mesenteric fat of obese individuals. Ralstonia pickettii worsened glucose tolerance and increased endotoxin in mice, suggesting a role in metabolic disease.

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Area of Science:

  • Microbiology
  • Metabolic Disease Research
  • Gut Microbiome Studies

Background:

  • Altered gut microbiota is linked to metabolic diseases like obesity and type 2 diabetes mellitus (T2DM).
  • Low-grade inflammation, potentially driven by gut bacteria, may cause insulin resistance in obesity.

Purpose of the Study:

  • To investigate the presence of bacterial DNA in mesenteric adipose tissue of obese humans.
  • To determine the role of Ralstonia pickettii in the development of obesity and T2DM.

Main Methods:

  • Pyrosequencing of bacterial 16S rRNA genes to identify bacteria in mesenteric adipose tissue.
  • Fecal abundance analysis of Ralstonia pickettii in human subjects.
  • A proof-of-concept study in diet-induced obese (DIO) mice treated with R. pickettii.

Main Results:

  • Bacterial DNA, predominantly from Ralstonia, was detected in mesenteric adipose tissue of obese subjects.
  • Fecal abundance of Ralstonia pickettii was elevated in obese subjects with pre-diabetes and T2DM.
  • R. pickettii treatment in DIO mice led to impaired glucose tolerance and increased circulating endotoxin levels.

Conclusions:

  • Intestinal Ralstonia is more prevalent in obese human subjects with T2DM.
  • Ralstonia pickettii exacerbates glucose intolerance in diet-induced obese mice, indicating a potential causal role in metabolic dysfunction.