Infant malnutrition and poor sanitation damages intestinal ecosystem even if diet improves: Mice data

Even moderate malnutrition in the young coupled with poor sanitation is enough to provoke environmental enteropathy (EE), a condition that debilitates the digestive system so that even if the diet improves, nutritional uptake remains compromised.

This is the conclusion of a mice study published in Nature Communications that describes a vicious circle of malnutrition damaging the body’s capacity to process nutrients. Malnutrition causes 20% of under-5 deaths across the world.

Canadian researchers, led by professor Brett Finlay from the Department of Microbiology and Immunology at the University of British Columbia in Vancouver, found mouse pups fed a ‘moderately malnourished diet’ developed EE symptoms when simultaneously exposed to faecal-associated bacteria (to simulate unsanitary conditions).

Later feeding the mice pups normal diets for 21 days still resulted in 30% stunted growth as well as retarded protein uptake and increased small intestine permeability.

"The metabolomic analysis of the small intestine revealed for the first time that malnutrition leads to drastic shifts in small intestinal bile acid pool," they wrote. "Specifically, a reduction in tauroconjugated bile acids was observed in malnourished mice, which are important for fat and nutrient uptake in the small intestine."

They added that such a bile deficiency could be linked to "observed alterations in the luminal bioavailability of the fat-soluble vitamins A, D and E."

Changes in bile composition could foster colonisation by Bacteroidales and E. coli strains in the small intestine, they suggested.

Finlay and the researchers suggested the intestinal microflora had been altered by the introduced bacterium but said more research was required to understand the particular mechanism of action.

Source:

Nature Communications

August 4 (DOI:10.1038/ncomms8806)

‘Diet and specific microbial exposure trigger features of environmental enteropathy in a novel murine model’

Authors:  B Brett Finlay et al