Leaky Gut as a Potential Culprit for the Paradoxical Dysglycemic Response to Gastric Bypass-Associated Ileal Microbiota

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Leaky Gut as a Potential Culprit for the Paradoxical Dysglycemic Response to Gastric Bypass-Associated Ileal Microbiota. / Hankir, Mohammed K.; Seyfried, Florian; Schellinger, Isabel N.; Schlegel, Nicolas; Arora, Tulika.

In: Metabolites, Vol. 11, No. 3, 153, 2021.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Hankir, MK, Seyfried, F, Schellinger, IN, Schlegel, N & Arora, T 2021, 'Leaky Gut as a Potential Culprit for the Paradoxical Dysglycemic Response to Gastric Bypass-Associated Ileal Microbiota', Metabolites, vol. 11, no. 3, 153. https://doi.org/10.3390/metabo11030153

APA

Hankir, M. K., Seyfried, F., Schellinger, I. N., Schlegel, N., & Arora, T. (2021). Leaky Gut as a Potential Culprit for the Paradoxical Dysglycemic Response to Gastric Bypass-Associated Ileal Microbiota. Metabolites, 11(3), [153]. https://doi.org/10.3390/metabo11030153

Vancouver

Hankir MK, Seyfried F, Schellinger IN, Schlegel N, Arora T. Leaky Gut as a Potential Culprit for the Paradoxical Dysglycemic Response to Gastric Bypass-Associated Ileal Microbiota. Metabolites. 2021;11(3). 153. https://doi.org/10.3390/metabo11030153

Author

Hankir, Mohammed K. ; Seyfried, Florian ; Schellinger, Isabel N. ; Schlegel, Nicolas ; Arora, Tulika. / Leaky Gut as a Potential Culprit for the Paradoxical Dysglycemic Response to Gastric Bypass-Associated Ileal Microbiota. In: Metabolites. 2021 ; Vol. 11, No. 3.

Bibtex

@article{1b56cdef82df47349c26209d0c0c750c,
title = "Leaky Gut as a Potential Culprit for the Paradoxical Dysglycemic Response to Gastric Bypass-Associated Ileal Microbiota",
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 sol-uble 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.",
keywords = "Intestinal epithelial barrier, Intestinal microbiota, Roux-en-Y gastric bypass surgery, Systemic endotoxemia, Type 2 diabetes",
author = "Hankir, {Mohammed K.} and Florian Seyfried and Schellinger, {Isabel N.} and Nicolas Schlegel and Tulika Arora",
year = "2021",
doi = "10.3390/metabo11030153",
language = "English",
volume = "11",
journal = "Metabolites",
issn = "2218-1989",
publisher = "M D P I AG",
number = "3",

}

RIS

TY - JOUR

T1 - Leaky Gut as a Potential Culprit for the Paradoxical Dysglycemic Response to Gastric Bypass-Associated Ileal Microbiota

AU - Hankir, Mohammed K.

AU - Seyfried, Florian

AU - Schellinger, Isabel N.

AU - Schlegel, Nicolas

AU - Arora, Tulika

PY - 2021

Y1 - 2021

N2 - 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 sol-uble 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.

AB - 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 sol-uble 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.

KW - Intestinal epithelial barrier

KW - Intestinal microbiota

KW - Roux-en-Y gastric bypass surgery

KW - Systemic endotoxemia

KW - Type 2 diabetes

U2 - 10.3390/metabo11030153

DO - 10.3390/metabo11030153

M3 - Journal article

C2 - 33800456

AN - SCOPUS:85103016127

VL - 11

JO - Metabolites

JF - Metabolites

SN - 2218-1989

IS - 3

M1 - 153

ER -

ID: 259677257