The worldwide obesity epidemic is stimulating efforts to identify host and environmental factors that affect energy balance. Comparisons of the distal gut microbiota of genetically obese mice and their lean littermates, as well as those of obese and lean human volunteers have revealed that obesity is associated with changes in the relative abundance of the two dominant bacterial divisions, the Bacteroidetes and the Firmicutes. Here we demonstrate through metagenomic and biochemical analyses that these changes affect the metabolic potential of the mouse gut microbiota. Our results indicate that the obese microbiome has an increased capacity to harvest energy from the diet. Furthermore, this trait is transmissible: colonization of germ-free mice with an 'obese microbiota' results in a significantly greater increase in total body fat than colonization with a 'lean microbiota'. These results identify the gut microbiota as an additional contributing factor to the pathophysiology of obesity.
Long-term diet influences the structure and activity of the trillions of
microorganisms residing in the human gut1–5, but it
remains unclear how rapidly and reproducibly the human gut microbiome responds
to short-term macronutrient change. Here, we show that the short-term
consumption of diets composed entirely of animal or plant products alters
microbial community structure and overwhelms inter-individual differences in
microbial gene expression. The animal-based diet increased the abundance of
bile-tolerant microorganisms (Alistipes, Bilophila, and
Bacteroides) and decreased the levels of Firmicutes that
metabolize dietary plant polysaccharides (Roseburia, Eubacterium
rectale, and Ruminococcus bromii). Microbial
activity mirrored differences between herbivorous and carnivorous
mammals2, reflecting
trade-offs between carbohydrate and protein fermentation. Foodborne microbes
from both diets transiently colonized the gut, including bacteria, fungi, and
even viruses. Finally, increases in the abundance and activity of
Bilophila wadsworthia on the animal-based diet support a
link between dietary fat, bile acids, and the outgrowth of microorganisms
capable of triggering inflammatory bowel disease6. In concert, these results demonstrate that the
gut microbiome can rapidly respond to altered diet, potentially facilitating the
diversity of human dietary lifestyles.
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