Gut Bacteria and Diabetes: Progress on Several Fronts

Several new studies have recently been published examining the relationship between gut bacteria and diabetes.  With one in ten people in the United States suffering from diabetes (which doesn’t include those with metabolic syndrome/insulin resistance, which would greatly inflate that number), we desperately need research in this area.

The first study was a meta analysis out of Oregon State University, published in the Lancet’s journal, EBioMedicine.[i] Scientists analyzed 42 studies on humans, and found that while there was no definitive consensus among them, there were some fairly consistent trends.  Firstly, Bacteroides and Bifidobacterium appear to be protective against type 2 diabetes (TD2): in all but one study, Bifido were found to be high in healthy controls and low in those with TD2.  The results regarding Lactobacillus species were very mixed:  L. acidophilus, L. gasseri and L. salivarius seem to be high in those with TD2, while other species in the family were low.  I found this an interesting concept:  11 studies showed that Lactobacillus have positive effect when combined with other bacteria, like Bifidobacterium.  Thus, researchers suspect that different families of bacteria work together in a synergistic way, protecting humans from developing diabetes.  Overall, they state, “Among the commonly and consistently reported findings, the genera of Bifidobacterium, Bacteroides, Faecalibacterium, Akkermansia and Roseburia were negatively associated with T2D, while the genera of Ruminococcus, Fusobacterium, and Blautia were positively associated with T2D.”

The second study looked at 40 people with severe obesity, half of whom had T2D, the other half of whom had normal blood glucose levels.[ii]  The researchers looked at samples of their blood, liver and 3 different kinds of fat tissue.  There were distinct differences between those with diabetes and those without.  In the liver and some fat tissues (the fat connecting the colon and stomach) from those with TD2, high levels of bacteria and bacterial fragments were found.  The thinking is that the increased inflammation from obesity causes leaky gut, allowing these out of the intestines.  This inflammatory process, in turn, prevents insulin from being able to do its job and remove glucose from the blood.  In fact, the bacteria found in those with TD2 are often from environmental sources:

“Our results find support in previous studies that report bacterial colonisation in blood and tissues in healthy and disease states, and further suggest that environmental bacteria, which are likely to be present in food and water, may cross the gut barrier to accumulate in the blood and organs. Most environmental bacteria that are increasingly found to be present in patients with T2D can be linked to …infections that are often distributed via hospital water supplies.  Because patients with diabetes are usually more frequently hospitalised than their counterparts without diabetes, they are at greater risk of contracting infections and therefore may acquire part of their tissue microbiota during such visits.”

They conclude that more research is needed, obviously, but that “These findings support the hypothesis that environmental bacteria can reach specific niches at various body sites and potentially influence glycaemic control.”

The third study was conducted collaboratively between McGill University in Canada, Kyoto University in Japan, and INSERM/University of Paris, in France.[iii]  These scientists looked at blood samples from 148 people and found one particular bacterial metabolite, 4-Cresol, appears to be a potential biomarker for resistance to developing diabetes: it is consistenly found in lower levels in the blood of those with diabetes. In animal studies, low doses of it cause an increase in pancreatic beta cells that produce insulin and reducing obesity.

4-Cresol is produced by a variety of gut bacteria, and is also a product of the fermentation of the amino acids, tyrosine and phenylalanine.  It’s also found at low levels in certain foods, including tomatoes, asparagus, wine, dairy, coffee and tea, and even ground water.  It appears to downregulate proinflammatory cytokines and to upregulate regulatory (anti-inflammatory) cytokines.

The lead researcher in this last study is quoted as saying, “Our goal is to develop therapeutic approaches that allow fine modulation of the intestinal flora, by promoting the proliferation of ‘good’ bacteria whose function is well understood and thus the production of bacterial metabolites at therapeutic doses…”[iv]

Sounds good to me.

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[i] Gurung, M, et. Al.  Role of gut microbiota in type 2  diabetes pathology. EBioMedicine. 2020;51:102590. OI:https://doi.org/10.1016/j.ebiom.2019.11.051

 

[ii] Anhê, F.F., Jensen, B.A.H., Varin, T.V. et al. Type 2 diabetes influences bacterial tissue compartmentalisation in human obesity. Nat Metab 2, 233–242 (2020). https://doi.org/10.1038/s42255-020-0178-9

 

[iii] Brial, F, et. Al. The natural metabolite 4-cresol improves glucose homeostasis and enhances B-cell function. Cell Reports. 2020;30(7):2306-2320. DOI:https://doi.org/10.1016/j.celrep.2020.01.066

[iv] https://newatlas.com/science/gut-microbiome-bacteria-diabetes-metastudy-metabolism/