Microbiota in obesity: interactions with enteroendocrine, immune and central nervous systems.
Mulders RJ, de Git KCG, Schéle E, Dickson SL, Sanz Y, Adan RAH
Obes Rev. Apr 2018. doi: 10.1111/obr.12661
COMMENT: One popular theory for the diet-induced obesity pandemia, for which there is a considerable evidence base, implicates the composition of intestinal microbiota and its genome (microbiome) which are modifiable by the diet.
It now seems clear that high-fat diets cause obesity, at least in part, by modifying the composition and function of the microorganisms that colonize in the gastrointestinal tract, the microbiota. The exact pathways by which intestinal microbiota contribute to obesity remain largely unknown.
High-fat diet-induced alterations in intestinal microbiota have been suggested to:
- increase energy extraction,
- intestinal permeability and systemic inflammation
- decreasing the capability to generate obesity-suppressing short-chain fatty acids.
Moreover by increasing systemic inflammation, microglial activation and affecting vagal nerve activity, 'obese microbiota' indirectly influence hypothalamic gene expression and promote overeating.
It is suggested that Akkermansia muciniphila, Bifidobacterium spp., Bacteroides uniformis and Clostridium coccoides may protect from obesity, based on their associations with adiposity, glycaemic control and leptin levels.
Conversely, Bilophila wadsworthia and Oscillibacter spp. are suggested to contribute to the pathogenesis of obesity. Moreover, bacterial taxa that become more abundant as a result of High-fat diet feeding can be tentatively identified as contributors to an obese phenotype, predictors of the susceptibility for developing obesity and as targets for intervention to prevent or treat obesity.
Nevertheless, as the authors of this review suggest:
prospective studies in humans and interventions with appropriate design are still needed to establish whether or not enhancing or suppressing specific bacterial groups can prevent or treat obesity.