Starch rich diets can influence the gut-microbiome and subsequently behavior

The microbiome’s role in modulating the gut-brain axis has been well-supported by a large body of evidence.  Many experiments in the past have demonstrated this in preclinical models by administering probiotics with specific bacterial strains or by fecal microbiome transplant in rodent models, which were then associated with changes in behavior.  Diet has also been implicated in these modulations, as food intake can influence species diversity and composition.  Low-digestible carbohydrates, or resistant starch, have received attention as being beneficial toward health, as these components are not digested but rather fermented by resident microbiota to produce an array of beneficial metabolites.  In a recent study, researchers from Texas Tech University investigated whether a diet rich in resistant starches were also associated with changes in behavior.

48 mice were randomly assigned to 3 different treatment groups, with each group either fed normal corn starch diet, a resistance starch rich diet, or an octenyl-succinate diet for 6 weeks.  The animals were monitored for weight, were subject to robust behavioral tests, and fecal samples were examined for microbiota composition.  The animals on the resistant starch diet exhibited similar weight gains as compared to the normal corn starch diet, and the octenyl-succinate group demonstrated lower weight gain.  Fecal microbiota analysis revealed diet correspondence to specific diet, and that resistant starch diet groups displayed increases in Verrucomicrobia and Actinobacteria as compared to octenyl-succinate and normal corn starch group, respectively.  In all groups, mice displayed significant anxiety-like-behavior in an elevated plus maze, and in open-field tests the mice fed resistance starch rich and octenyl-succinate diet mice exhibited high-anxiety-like behaviors. 

This data again supports that diet manipulation can have marked influence on behavior, and that starch rich diets could perhaps induce undesirable behavioral effect via modulation of the gut-brain axis.  This could be an important drawback to the beneficial components provided for microbial fermentation.  

Exposure to the cold affects our microbiome and modulates our energy homeostasis

When exposed to cold temperatures, you begin shivering to compensate for the sudden temperature decrease.  Biologically, exposure to cold environment can induce brown adipose tissue differentiation and catabolism of lipids to produce heat.  The gastrointestinal tract is an important site for the regulation of our energy metabolism, and as we know, harbors a diverse population of gut bacteria.  A team of researchers sought to investigate what role the microbiome of mice plays in induction of physiological changes to cold exposure.

The researchers exposed different groups of mice to cold temperatures for 31 days, and the initial observation was attenuation of energy expenditure and white fat.  Importantly, food intake was consistent throughout the trial, pointing to a temperature-driven effect.  Fecal collection and post-mortem intestinal analysis revealed marked shifts in microbiota compositions of cold-exposed mice as compared to those kept at room temperature.  Notably, families within Actinobacteria, Verrucomicrobia, and Tenericutes were less abundant in the cold sample mice, and Akkermansia muciniphila species were observed to be significantly decreased in the cold mice.  The researchers also transplanted microbiota from cold-group mice to naïve, germ-free mice.  Upon cold temperature exposure, germ-free mice demonstrated heightened insulin sensitivity, browning of white fat, increased energy expenditure, and white fat loss, indicative of a tolerance to the cold.  Prolonged cold exposure in both cold-exposed and cold-transplanted mice also induced adaptive biological mechanisms in intestinal villi and microvilli to maximize caloric uptake, ultimately attenuating weight loss.  This increase in intestinal absorption was observed concomitant to altered intestinal gene expression, as genes that promote tissue remodeling where upregulated while apoptotic genes were suppressed.  In a final experiment, the aforementioned effect was reduced when Akkermansia muciniphila (which were originally observed to decrease in cold-induced mice) were transplanted to cold-exposed mice, supporting a microbiota-driven relationship.

This was a very interesting study that sheds lights on organismal adaptive mechanisms during energy scarcity brought on by factors such as cold temperatures.  Again we observe heavy involvement of the microbiome in these processes, a finding that calls for more investigation.