Gut microbial adaptation to dietary consumption offructose, artificial sweeteners and sugar alcohols:implications for host–microbe interactionscontributing to obesity

The Western diet, comprised of highly refined carbohydrates and fat but reduced complex plant polysaccharides, has been attributed to the prevalence of obesity. A concomitant rise in the consumption of fructose and sugar substitutes such as sugar alcohols, artificial sweeteners, even rare sugars, has mirrored this trend, as both probable contributor and solution to the epidemic. Acknowledgement of the gut microbiota as a factor involved in obesity has sparked much controversy as to the cause and consequence of this relationship. Dietary intakes are a known modulator of gut microbial phylogeny and metabolic activity, frequently exploited to stimulate beneficial bacteria, promoting health benefits. Comparably little research exists on the impact of ‘unconscious’ dietary modulation on the resident commensal community mediated by increased fructose and sugar substitute consumption. This review highlights mechanisms of potential host and gut microbial fructose and sugar substitute metabolism. Evidence is presented suggesting these sugar compounds, particularly fructose, condition the microbiota, resulting in acquisition of a westernized microbiome with altered metabolic capacity. Disturbances in host–microbe interactions resulting from fructose consumption are also explored.

http://www.scribd.com/doc/99217193/Gut-Microbial-Adaptation

Continuous exposure to fructose and sugar substitutes may cause dysbiosis with loss of microbial genetic andphylogenic diversity, promoting evolution and maintenance of a Western gut microbiome. In turn adaptive metabolismgenerates additional energy sources for the host, which mayfacilitate aberrant host–microbe interactions leading to per-turbed energy regulation and altered gut transit times withsubsequent enhancement of dietary energy extraction.These differences in microbial composition and metabolicactivity may ultimately be sensed by the innate and adap-tive immune system leading to intestinal inflammation withlater manifestation as endotoxemia. The combination of these processes can undoubtedly contribute to developmentof many metabolic disorders associated with obesity. Inconclusion, we suggest obesity treatment and preventioncould be effectively achieved by promoting intestinalhomeostasis through reintroduction of a balanced anddiverse diet.