metabolic disorder

The microbiome can protect against metabolic dysregulation brought on by disease

Pathogenic infections can lead to metabolic alterations that result in maladies such as cachexia, or muscle wasting.  Antibiotics can be prescribed to treat a variety of intestinal diseases or inflammatory conditions, but these agents can also disrupt the natural microbiome ecology that could perhaps provide benefits to protecting against metabolic dysregulations.  On top of this, harnessing components of the microbiome with respect disease tolerance is an avenue under continuous exploration.  Within this contextual framework, researchers from The Salk Institute for Biological Studies in La Jolla, CA investigated to see whether components of the microbiome could have a protective effect on metabolic dysregulation brought on by gut trauma and/or infection.   

To initiate the investigation, the researchers used an induced-injury model known as the dextran sulfate sodium (DSS) intestinal injury model to create symptoms associated with inflammatory bowel disease/Crohn’s disease.  DSS was applied to mice in two cohorts procured from two distinct laboratories (Jackson labs [Jax] and UC Berkeley lab [CB]).  This treatment was administered to C57 mice followed by an administration of an antibiotic cocktail of ampicillin, vancomycin, neomycin, and metronidazole (AVNM) to provide remedy for the injury.  The AVNM cocktail had no impact on the severity of DSS in mice procured from Jackson labs, whereas mice procured from UC Berkeley colonies demonstrated significantly less muscle wasting.  This observation led to the hypothesis that microbiota composition differences between both cohorts of mice drove this observation. 

After examining cecal content from AVNM-CB and AVNM-Jax mice, it was determined that the CB mice had a higher composition of E. coli compared to the Jax mice.  Building on the original supposition, the researchers then administered E. coli to Jax mice, and upon DSS administration, they demonstrated significantly less wasting pathology as compared to the vehicle control groups (i.e., DSS treatment without being administered E. coli).  The researchers further investigated whether E. coli had a protective effect in response to infectious microbes in addition to induced-DSS injury, and Jax mice were infected with Salmonella Typhimurium or Burkholderia thailandensis.  There was no significant difference in alterations in host metabolism, caloric uptake, or inflammation between E. coli-administered groups and controls.  However, the E. coli group demonstrated increased signaling in the insulin-like growth factor 1/phosphatidylinositol 3-kinase/AKT pathway in skeletal muscle, a pathway implicated in the prevention of muscle wasting.  This finding effectively provides mechanistic evidence of protecting against muscle wasting. 

Together, these findings provide additional evidence that support the microbiome’s role in tempering inflammatory disease or injury.  Further delineation of molecular pathways associated with these maladies will advance our understanding and treatment of disease.   

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The views expressed in the blog are solely those of the author of the blog and not necessarily the American Microbiome Institute or any of our scientists, sponsors, donors, or affiliates.

The fungal microbiome in obese individuals

We hear mostly about the bacterial microbiome but there are other microbiomes out there like the virome (virus microbiome) and mycobiome (fungal microbiome). The mycobiome is an important part of the gastrointestinal tract and fungal microorganisms make up between .03-2% of the total microorganisms in the gut. A recent study out of Spain characterized the mycobiome of obese individuals and compared them to non-obese individuals.

The scientists used sequencing technologies to analyze the diversity of fungal organisms in the gut of 52 Caucasian individuals who were recruited for the study. After fecal sampling and sequencing, they found that diversity was lower in obese subjects than in non-obese subjects and they could be stratified depending on their mycobiome composition. Ascomycota and Basidiomycota were not significantly different between the two groups, however, the minor phylum Zygomycota was represented less in obese patients.

Interestingly, they found that the relative abundance of fungus in the Eurotiomycetes class of the Ascomycota phylum were similar between obese individuals and non-obese individuals but obese subjects with low levels of Eurotiomycetes had worse metabolic profiles. These subjects were identified as more “unhealthy” obese subjects than those with a higher abundance of Eurotiomycetes. 

This was the first study to look at the human mycobiome in relation to obesity and associated metabolic disorders. Further knowledge of these interactions between the mycobiome, microbiome, and metabolic disorders may elucidate new methods for treating obesity and metabolic syndromes.  

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The views expressed in the blog are solely those of the author of the blog and not necessarily the American Microbiome Institute or any of our scientists, sponsors, donors, or affiliates.