@article{HankirSeyfriedSchellingeretal.2021,
  author    = {Hankir, Mohammed K. and Seyfried, Florian and Schellinger, Isabel N. and Schlegel, Nicolas and Arora, Tulika},
  title     = {Leaky gut as a potential culprit for the paradoxical dysglycemic response to gastric bypass-associated ileal microbiota},
  series = {Metabolites},
  volume    = {11},
  journal   = {Metabolites},
  number    = {3},
  issn      = {2218-1989},
  doi       = {10.3390/metabo11030153},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-234085},
  year      = {2021},
  abstract  = {Altered host-intestinal microbiota interactions are increasingly implicated in the metabolic benefits of Roux-en-Y gastric bypass (RYGB) surgery. We previously found, however, that RYGB-associated ileal microbiota can paradoxically impair host glycemic control when transferred to germ-free mice. Here we present complementary evidence suggesting that this could be due to the heightened development of systemic endotoxemia. Consistently, application of ileal content from RYGB-treated compared with sham-operated rats onto Caco-2 cell monolayers compromised barrier function and decreased expression of the barrier-stabilizing proteins claudin-4 and desmoglein-2. Our findings raise the possibility that RYGB-associated ileal microbiota produce and release soluble metabolites which locally increase intestinal permeability to promote systemic endotoxemia-induced insulin resistance, with potential implications for the treatment of RYGB patients who eventually relapse onto type 2 diabetes.},
  language  = {en}
}