• Human obesity causes an increase in the jejunal mucosal surface
  • Both innate and adaptive immune cells are increased in the gut in obesity
  • There is increased homing of CD8αβ T cells in the obese jejunum epithelium
  • T cells from obese subjects impair insulin sensitivity of enterocyte

There is a strong association between the gut microbiome and the human host.  Different characteristics of the microbiome, including bacterial diversity and the abundance of specific bacterial groups, may play a role in the development of obesity and related complications.  Among those, the role of the gut bacterial species Akkermansia muciniphila was highlighted for maintaining metabolic health in mouse models.

Because little is known in humans, Karine Clément’s team at Institute of Cardiometabolism and Nutrition (INSERM- University Pierre et Marie Curie), have explored the link between markers of human health, diet, microbiota and the intestinal abundance of Akkermansia muciniphila in 49 overweight and obese subjects. 

They found that intestinal A. muciniphila is associated with better insulin sensitivity. Obese subjects that initially had higher abundance of A. muciniphila experienced greater benefits from calorie restriction in terms of waist circumference and cholesterol reduction, and insulin sensitivity improvement.  

Most importantly, the healthiest participants before and after the intervention not only had more A. muciniphila but also the most diverse repertoire of bacterial species in the gut.  These results demonstrate the importance of studying the gut microbiome as an ecosystem rather than having a narrow focus on specific bacterial groups.  Further, our findings support future investigation of A. muciniphila as a potential marker or therapeutic target of obesity-related diseases.   

Microbiome research is actively advancing to address the many questions that remain regarding its relationship with human health.  An integrative approach is required for this investigation because the microbiome interacts with the host and the environment in the development of obesity and its co-morbidities.  So far, evidence suggests that health may be restored partly through modification of the gut ecosystem, and therefore it is critical to identify gut microbial patterns and signatures that characterize different stages of disease and may help in their diagnosis, treatment and prevention.

Gene content differences in human gut microbes can lead to inter-individual phenotypic variations such as digestive capacity. It is unclear whether gene content variation is caused by differences in microbial species composition or by the presence of different strains of the same species; the extent of gene content variation in the latter is unknown. Unlike pan-genome studies of cultivable strains, the use of metagenomic data can provide an unbiased view of structural variation of gut bacterial strains by measuring them in their natural habitats, the gut of each individual in this case, representing native boundaries between gut bacterial populations. We analyzed publicly available metagenomic data from fecal samples to characterize inter-individual variation in gut bacterial species.                                                                                                                                                                                            

We wanted to discover whether different eating patterns in obese and overweight patients affected how inflammation parameters and gut microbiota composition might change. We found some variation between groups of different weight. It's unclear what relates to what (in terms of weight, gut microbes and inflammation). The results are published in PLOS One.

Having a catalog of reference genes is a really important step to take in terms of successfully analyzing the gut microbiome. Existing catalogs are based on samples from single cohorts or reference genomes meaning that coverage is potentially limited for our purposes. As such we decided to combine some pre-existing catalogs into one source and so, we now have a catalog of just short of 10 million genes. We published this work in Nature Biotechnology.

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