Prevotella in the gut appears to improve glucose tolerance

Last week we wrote about a study that showed that the glycemic response from foods was a function of the microbiome, and alluded to the fact that the microbiome likely affects many aspects of metabolism.  Another paper was published this week, in the journal Cell Metabolism, that describes which bacteria are responsible for some of these effects.  The authors describe how Prevotella improve glucose metabolism in healthy human subjects.

The scientists gave 39 subjects white bread and barley bread for three consecutive days and measured their glucose and insulin responses to the diets.  For the most part, the barley bread was associated with an improved response over white bread, but some of the individuals’ responded with a much more stark improvement than others.  The scientists then measured the gut microbiomes of each individual and noted that the microbiome changed in the most responsive individuals, and this change was characterized by an increase in Prevotella (specifically Prevotella copri) and methanogenic archaea.  The opposite effect was seen in the individuals that responded least to the barley bread intervention.  The scientists then confirmed these results in mice.  Mice that were given fecal microbiota transplants from human responders, or P. copri probiotics had improved glycemic responses to high fiber diets than control mice.

Prevotella comes up in a lot of microbiome literature as a bug seen in ‘traditional’ societies that eat a lot of fiber.  This paper demonstrates that many of the genes from Prevotella are crucial to digest the complex fibers and that this may stimulate an improved glycemic response.  Collectively, many papers now support the idea that Prevotella is a critical bacterium to a ‘healthy’ microbiome.

Gut microbiome depletion promotes healthier brown fat and reduces obesity in mice

The white and brown turkey meat from a Thanksgiving dinner

An interesting article from Switzerland was published last week in Nature Medicine.  The scientists reported on a new connection between the gut microbiome and metabolic syndrome (i.e. insulin sensitivity, obesity, etc.)  Whereas most papers observe microbiome disruption and depletion is associated with obesity, this paper describes a different phenomenon: that mice with depleted microbiomes are metabolically healthier than their untouched microbiome counterparts.  As part of the basis for the paper it is important to understand that mammals have two types of fat, brown fat and white fat.  Brown fat is associated with exercise, insulin sensitivity, and health, and white fat is associated with insulin resistance and diabetes.  Brown fat can actually repopulate white fat in a process called browning, and this transition is healthy.  

In the study, the scientists started with either normal mice, germ free mice, or mice that had antibiotics administered to them. They challenged each group of mice with glucose, and noted that antibiotic administration led to improved insulin sensitivity.  When they investigated where the glucose was going, they discovered that it was uptaken by white adipose tissue under the skin.  Then, they compared the normal mice and antibiotic mice, and observed that the antibiotic mice actually had smaller volumes of fat after the glucose uptake.  Interestingly, the fat cells in the germ free and antibiotic mice were smaller and more dense, whereas the normal mice had fewer, larger cells.  The researchers then confirmed that browning of fat was occurring in the germ free and antibiotic mice.  Finally, when the scientists transplanted the microbiome of normal mice into the germ free mice a reversal of many the above described characteristics occurred.  In these mice the fat stopped browning, insulin resistance decreased, and the mice gained weight.

The scientists were able to attribute some of the above phenomena to the release of specific cytokines (molecules that regulate the immune system).  This paper, then, adds to the wealth of research that describes the complex but critical interaction between the gut microbiome, the immune system, and metabolic syndrome.  Although the relationships between these things is yet to be fully understood, this paper may at least change the way you think about the dark and white meat during Thanksgiving dinner this Thursday.

Too much jetlag may contribute to obesity

A study published last week in Cell explores the microbiome of the gut in both mice and humans, and it’s responses to changes in its biological rhythm. Researchers performed many experiments that were comprised of altering the dark-light conditions in which mice were kept, as well as the feeding times of mice.

Many important results were found from the multiple variations in experimental conditions to which the researchers subjected the mice. First, researchers uncovered that the microbiome has time-of-day- specific differences in function and composition. Evidence suggests that feeding patterns dictate this fluctuation. After mimicking jet-lag in mice, compared to a control group, these mice exhibited imbalances in their gut microbiome. It was later found that this imbalance could be transferable from jet-lagged mice to mice raised germ-free, through the fecal transfer of the gut microbiome. An experiment was also done in which jet-lagged and control group mice were fed high fat diets. The jet-lagged mice exhibited enhanced weight gain and glucose intolerance. Antibiotic treatment showed a decrease in these symptoms. Lastly, a study was done in humans who were subjected to jet-lag, which suggested that the microbiome of humans also undergoes daily oscillations, and that disruption of this rhythm can lead to imbalances in the microbiome and in human metabolism. The human study was only done with two individuals and fortunately, their microbiomes returned to normal after just two weeks though still raising questions about the impact that too much travel and jet-lag could have on health.

The experiments done in this study opens the door for further research on the microbiome’s sensitivity to changes in a human’s biological clock, as well as the impacted microbiome’s influence on the metabolism of its host.