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Roux-en-Y gastric bypass potentially improved intestinal permeability by regulating gut innate immunity in diet-induced obese mice.

ABSTRACT: Roux-en-Y gastric bypass (RYGB) has been demonstrated to be the most effective treatment for morbid obesity, yet the impact of RYGB on intestinal permeability is not fully known. In this work, we subjected obese mice to RYGB and sham operation procedures. Serum lipopolysaccharide (LPS) level, inflammatory cytokines and intestinal permeability were measured at 8 weeks post surgery. In contrast to sham surgery, RYGB reduced body weight, improved glucose tolerance and insulin resistance, and decreased serum levels of LPS, IL6 and TNFα. Intestinal permeability of the common limb and colon was significantly improved in the RYGB group compared to the sham group. The mRNA levels of IL1β, IL6, and TLR4 in the intestine were significantly decreased in the RYGB group compared with the sham group. The expression levels of intestinal islet-derived 3β (REG3β), islet-derived 3γ (REG3γ) and intestinal alkaline phosphatase (IAP) were higher in the RYGB group than in the sham group. In conclusion, in a diet-induced obesity (DIO) mouse model, both decreased intestinal permeability and attenuated systemic inflammation after RYGB surgery were associated with improved innate immunity, which might result from enhanced production of IAP and antimicrobial peptides.

SUBMITTER: Jin Z

PROVIDER: S-EPMC8295358 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Goto-Kakizaki rats with Roux-en-Y gastric bypass surgery

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Management of a refractory marginal ulcer following Roux-en-Y gastric bypass with EUS-guided Roux-en-Y gastric bypass reversal.

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Reprogramming of defended body weight after Roux-En-Y gastric bypass surgery in diet-induced obese mice.

Project description:ObjectiveRoux-en-Y gastric bypass surgery (RYGB) results in sustained lowering of body weight in most patients, but the mechanisms involved are poorly understood. The aim of this study was to obtain support for the notion that reprogramming of defended body weight, rather than passive restriction of energy intake, is a fundamental mechanism of RYGB.MethodsMale C57BL6J mice reaching different degrees of obesity on a high-fat diet either with ad libitum access or with caloric restriction (weight-reduced) were subjected to RYGB.ResultsRYGB-induced weight loss and fat mass loss were proportional to pre-surgical levels, with moderately obese mice losing less body weight and fat compared with very obese mice. Remarkably, mice that were weight-reduced to the level of chow controls before surgery immediately gained weight after surgery, exclusively accounted for by lean mass gain.ConclusionsThe results provide additional evidence for reprogramming of a new defended body weight as an important principle by which RYGB lastingly suppresses body weight. RYGB appears to selectively abolish defense of a higher fat mass level, while remaining sensitive to the defense of lean mass. The molecular and physiological mechanisms underlying this reprogramming remain to be elucidated.

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Should Roux-en-Y gastric bypass biliopancreatic limb length be tailored to achieve improved diabetes outcomes?

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Global Transcriptional Profiling of Women Following Roux-en-Y Gastric Bypass

Project description:Analysis of changes in gene expression after weight loss. The hypothesis tested in this study was that the weight loss caused by Roux-en-Y Gastric bypass may alter the expression of genes involved in multiple molecular pathways related to obesity. The results will generate important data for studies involving treatment of obesity, which is characterized as a multifactorial disease that affects thousands of individuals worldwide.

2017-09-03 | GSE83223 | GEO

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