Sugar {51111159}

Shared Reference Notes

• [1.1] 
  - The abundance of the mucus-degrading bacteria Akkermansia muciniphila and Bacteroides fragilis was increased. - Bacteria-derived mucolytic enzymes were enriched leading to erosion of the colonic mucus layer of sugar-fed mice. - Sugar-induced exacerbation of colitis was not observed when mice were treated with antibiotics or maintained in a germ-free environment, suggesting that altered microbiota played a critical role in sugar-induced colitis pathogenesis.
• [1.2] [#Ulcerative Colitis] [#Plant-based diet] 
  - A positive association between a “high sugar and soft drinks” pattern and UC risk - When considering the foods most associated with the pattern, high consumers of sugar and soft drinks were at higher UC risk only if they had low vegetables intakes.
• [1.3] [#Inflamatory bowel disease] 
  - A sugar-rich diet favors the increase of #Akkermansia muciniphila, a mucolytic bacterium. The mucus layer separates luminal bacteria from intestinal epithelium: A thinner mucus layer allows bacteria to come in contact with the epithelial cells, eliciting an inflammatory response.
• - A sugar-rich diet increases the percentage of pro-inflammatory Sutterellaceae and Marinilabiliaceae, which induce bowel inflammation, and reduce bacteria with anti-inflammatory properties like Lachnospiraceae and Lactobacillaceae, able to produce the short-chain fatty acid (SCFA) butyrate, the main anergy source of enterocytes.
• [1.4] 
  - #Butyrate inhibits gut microbiome #Bacteroides - #Butyrate inhibition depends on which sugar a given #Bacteroides strain uses - Core genome variation in Acyl-CoA enzymes mediates #Butyrate defense - Each #Bacteroides unique fitness landscape unpredictable by interaction of ecosystem parts
• [1.5] [#Prediabetes] [#High-fat diet] 
  - microbiota protects against development of #Obesity, #Metabolic syndrome, and pre-diabetic phenotypes by inducing commensal-specific Th17 cells. - High-fat, high-sugar diet promoted metabolic disease by depleting Th17-inducing microbes, and recovery of commensal Th17 cells restored protection. - Diet-induced loss of protective Th17 cells was mediated by the presence of sugar. - Eliminating sugar from high-fat diets protected mice from #Obesity and #Metabolic syndrome in a manner dependent on commensal-specific Th17 cells. - Sugar and ILC3 promoted outgrowth of #Faecalibaculum rodentium that displaced Th17-inducing microbiota.

References Notes